Poisoning the Mitochondria
- Thread starter Radio
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Sulfite Oxidase enzyme deficiency is a very rare condition and the consequences are way more severe than CFS
Hey Elph86,
If you study my posts you will see that there are many ways Sulfite Oxidase can be impacted...Functional SUOX (B-12) Deficiency.....Molybdenum Deficiency....MOCS1, MOCS2 genes....Mercury exposure...Yes (dysbiosis) could be a factor....Thanks for pointing that out...In my opinion MTR/MTRR, H-pylori and environmental poisons are the main factors.
Dr. Amy Yasko, "Sulfate levels may be used as a way to assess sulfite processing. Sulfites are converted to sulfates by SUOX which uses B12 and molybdenum in the reaction"
Low sulfate can occur for a variety of reasons. Some gut infections (bacteria/yeast) can produce large amounts of phenols....which may overload the PST enzyme....causing a shortage of available sulfate.
The main reason for low functioning PST is low sulfate in the body. Sulfate is essential to keep PST functioning....sulfate is also necessary in maintaing the integrity of the intestinal lining. Low sulfate levels = increased intestinal permeability (leaky gut).
Hey Elph86,
If you study my posts you will see that there are many ways Sulfite Oxidase can be impacted...Functional SUOX (B-12) Deficiency.....Molybdenum Deficiency....MOCS1, MOCS2 genes....Mercury exposure...Yes (dysbiosis) could be a factor....Thanks for pointing that out...In my opinion MTR/MTRR, H-pylori and environmental poisons are the main factors.
Dr. Amy Yasko, "Sulfate levels may be used as a way to assess sulfite processing. Sulfites are converted to sulfates by SUOX which uses B12 and molybdenum in the reaction"
Low sulfate can occur for a variety of reasons. Some gut infections (bacteria/yeast) can produce large amounts of phenols....which may overload the PST enzyme....causing a shortage of available sulfate.
The main reason for low functioning PST is low sulfate in the body. Sulfate is essential to keep PST functioning....sulfate is also necessary in maintaing the integrity of the intestinal lining. Low sulfate levels = increased intestinal permeability (leaky gut).
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Magnesium Injections: The standard procedure for magnesium injections involves magnesium sulphate (which requires a prescription) being administered intramuscularly 1gm/2mls weekly for 10 weeks. Approximately 70% of Dr. Myhill’s CFS patients improve based on this protocol. Oral thiamine may help the magnesium be absorbed by patient’s cells and a calcium supplement may aid avoidance of a mineral imbalance. Many CFS specialists believe that despite CFS patients having normal blood levels of magnesium, patients have low intracellular magnesium levels.
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Rand56
Senior Member
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- Location
- Myrtle Beach, SC
Hi Radio
You'll have to excuse my question here because it stems from my lack of biochemistry knowledge, so maybe you can help answer a question.
In one of Dr. Seneff's podcasts I listened to, she mentioned that Resveratrol, Curcumin, polyphenols, and flavonoids help with sulfate transport within the body.
If this is a good thing, then what is the difference between polyphenols and phenols, besides their molecular makeup? In your post above it states that excess phenols is not a good thing, so hence my question.
Hey Rand,
In a normal body that has the correct levels of sulphates and liver enzymes, phenols and salicylates are easily metabolized. The body utilizes what it needs from the chemicals and properly disposes of the rest through the bowels. In those whose levels are not normal or in the case of leaky gut syndrome.... intolerance to this chemical family can occur rather quickly. Many people with gut issues such as yeast/bacteria overgrowth or digestive diseases can develop salicylate intolerance...
PST is a Phase II enzyme that detoxifies leftover hormones and a wide variety of toxic molecules, such as phenols and amines that are produced in the body and even in the gut by bacteria, yeast, and other fungi as well as food dyes and chemicals.These reactions include the breakdown of bilirubin and biliverdin...which are the breakdown products of hemoglobin. There are many varieties of phenols....The PST enzyme is only one of many sulfotransferases, and various other body chemicals...Sulfate must be grabbed by any sulfotransferase before the enzyme can attach it to something else, like phenols <--- That's the problem...We need Sulfates for the PST enzyme to work.
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RichVank,
"I've seen a couple of papers about low blood sulfate in autism, as well as one on low DHEA-sulfate. Also, I do know that mercury can block the sulfate transporters that normally reabsorb sulfate in the kidneys, so if there is high mercury in the kidneys, I think that sulfate wasting would occur."
"As I wrote in an earlier post, I suspect that the presence of sulfate-reducing bacteria in the gut would cause lower sulfate and elevated H2S in the urine."
"Some people with ME/CFS are low in sulfate. This is also true in autism, as published originally by Rosemary Waring. In both these disorders, there is a partial block in methionine sythase in the methylation cycle, and this causes too much of the homocysteine to be lost from the methylation cycle and instead to enter the transsulfuration cycle and pass through sulfoxidation to make sulfate, which then is excreted in the urine. The sulfate transporters in the kidneys can be blocked by mercury or other toxic metals, which build up because of glutathione depletion, and thus not enough sulfate is retained to do several important jobs, including sulfating DHEA, sulfating a range of toxins as part of Phase II detoxication, including phenols from certain foods, and supporting the cartilage in the joints. Some people take Epsom salt baths to raise their sulfate. Most can tolerate them, but a few can't. I suspect that these people have sulfate-reducing bacteria in their gut that convert sulfate to hydrogen sulfide, which is toxic at high enough levels. Fixing the methylation cycle block is the longer range solution to the sulfate deficiency problem."
Best regards,
Rich
Dr. Rosemary Waring found that most people with autism have a deficiency in a key detoxification pathway. The pathway involves using sulfur in the form of sulfate (known as sulfation). The enzyme involved is phenol sulfur-transferase (PST), but the problem is thought to hinge on an inadequate supply of usable sulfate ions, not the metabolic enzyme itself is essential for normal cellular function.
Dr. Rosemary Waring
http://www.autismcanada.org/treatments/biomed/sulfate.html
Sulfate reabsorption in the kidneys
The kidney plays a major role in sulfate homeostasis. Sulfate is freely filtered and then undergoes net reabsorption in the proximal tubule. The apical membrane Na+/sulfate cotransporter NaS1 (SLC13A1) has a major role in mediating proximal tubule sulfate reabsorption, as demonstrated by the findings of hyposulfatemia and hypersulfaturia in Nas1-null mice. The anion exchanger SAT1 (SLC26A1), the founding member of the SLC26 sulfate transporter family, mediates sulfate exit across the basolateral membrane to complete the process of transtubular sulfate reabsorption. Another member of this family, CFEX (SLC26A6), is present at the apical membrane of proximal tubular cells. It also can transport sulfate by anion exchange, which probably mediates backflux of sulfate into the lumen.
"I've seen a couple of papers about low blood sulfate in autism, as well as one on low DHEA-sulfate. Also, I do know that mercury can block the sulfate transporters that normally reabsorb sulfate in the kidneys, so if there is high mercury in the kidneys, I think that sulfate wasting would occur."
"As I wrote in an earlier post, I suspect that the presence of sulfate-reducing bacteria in the gut would cause lower sulfate and elevated H2S in the urine."
"Some people with ME/CFS are low in sulfate. This is also true in autism, as published originally by Rosemary Waring. In both these disorders, there is a partial block in methionine sythase in the methylation cycle, and this causes too much of the homocysteine to be lost from the methylation cycle and instead to enter the transsulfuration cycle and pass through sulfoxidation to make sulfate, which then is excreted in the urine. The sulfate transporters in the kidneys can be blocked by mercury or other toxic metals, which build up because of glutathione depletion, and thus not enough sulfate is retained to do several important jobs, including sulfating DHEA, sulfating a range of toxins as part of Phase II detoxication, including phenols from certain foods, and supporting the cartilage in the joints. Some people take Epsom salt baths to raise their sulfate. Most can tolerate them, but a few can't. I suspect that these people have sulfate-reducing bacteria in their gut that convert sulfate to hydrogen sulfide, which is toxic at high enough levels. Fixing the methylation cycle block is the longer range solution to the sulfate deficiency problem."
Best regards,
Rich
Dr. Rosemary Waring found that most people with autism have a deficiency in a key detoxification pathway. The pathway involves using sulfur in the form of sulfate (known as sulfation). The enzyme involved is phenol sulfur-transferase (PST), but the problem is thought to hinge on an inadequate supply of usable sulfate ions, not the metabolic enzyme itself is essential for normal cellular function.
Dr. Rosemary Waring
http://www.autismcanada.org/treatments/biomed/sulfate.html
Sulfate reabsorption in the kidneys
The kidney plays a major role in sulfate homeostasis. Sulfate is freely filtered and then undergoes net reabsorption in the proximal tubule. The apical membrane Na+/sulfate cotransporter NaS1 (SLC13A1) has a major role in mediating proximal tubule sulfate reabsorption, as demonstrated by the findings of hyposulfatemia and hypersulfaturia in Nas1-null mice. The anion exchanger SAT1 (SLC26A1), the founding member of the SLC26 sulfate transporter family, mediates sulfate exit across the basolateral membrane to complete the process of transtubular sulfate reabsorption. Another member of this family, CFEX (SLC26A6), is present at the apical membrane of proximal tubular cells. It also can transport sulfate by anion exchange, which probably mediates backflux of sulfate into the lumen.
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Mercury poisoning
Mercury irreversibly inhibits selenium-dependent enzymes and may also inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-o-methyl transferase. <--The COMT Problem.
Affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, and / or insomnia.
Mercury is unique among the heavy metals in that it can exist in several physical and chemical forms, including elemental mercury, which is a liquid at room temperature. All forms of mercury have toxic effects in a number of organs, especially in the kidneys. Within the kidney, the pars recta of the proximal tubule is the most vulnerable segment of the nephron to the toxic effects of mercury. The biological and toxicological activity of mercurous and mercuric ions in the kidney can be defined largely by the molecular interactions that occur at critical nucleophilic sites in and around target cells. Because of the high bonding affinity between mercury and sulfur, there is particular interest in the interactions that occur between mercuric ions and the thiol group(s) of proteins, peptides and amino acids. Molecular interactions with sulfhydryl groups in molecules of albumin, metallothionein, glutathione, and cysteine have been implicated in mechanisms involved in the proximal tubular uptake, accumulation, transport, and toxicity of mercuric ions. In addition, the susceptibility of target cells in the kidneys to the injurious effects of mercury is modified by a number of intracellular and extracellular factors relating to several thiol-containing molecules.
Smoking Teeth / Poison Gas
Trace minerals are essential for all of us. Besides their vital role in the health of our metabolism, they seem to be able to relocate heavy metals by mobilizing them and keeping them moving, eventually fining them an exit door. Listening to Ed Kane describe the process with BodyBio Liquid Minerals is not only interesting, but seems the only safe and healthy way to get the job done.
BodyBio Video Library - Trace Minerals Video Part One
http://www.bodybio.com/content.aspx?page=BodyBioWellnessVideoLibrary
Molecular interactions with mercury in the kidney
http://www.ncbi.nlm.nih.gov/pubmed/10699157
Mercury poisoning Wiki
http://en.wikipedia.org/wiki/Mercury_poisoning
Mercury irreversibly inhibits selenium-dependent enzymes and may also inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-o-methyl transferase. <--The COMT Problem.
Affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, and / or insomnia.
Mercury is unique among the heavy metals in that it can exist in several physical and chemical forms, including elemental mercury, which is a liquid at room temperature. All forms of mercury have toxic effects in a number of organs, especially in the kidneys. Within the kidney, the pars recta of the proximal tubule is the most vulnerable segment of the nephron to the toxic effects of mercury. The biological and toxicological activity of mercurous and mercuric ions in the kidney can be defined largely by the molecular interactions that occur at critical nucleophilic sites in and around target cells. Because of the high bonding affinity between mercury and sulfur, there is particular interest in the interactions that occur between mercuric ions and the thiol group(s) of proteins, peptides and amino acids. Molecular interactions with sulfhydryl groups in molecules of albumin, metallothionein, glutathione, and cysteine have been implicated in mechanisms involved in the proximal tubular uptake, accumulation, transport, and toxicity of mercuric ions. In addition, the susceptibility of target cells in the kidneys to the injurious effects of mercury is modified by a number of intracellular and extracellular factors relating to several thiol-containing molecules.
Smoking Teeth / Poison Gas
Trace minerals are essential for all of us. Besides their vital role in the health of our metabolism, they seem to be able to relocate heavy metals by mobilizing them and keeping them moving, eventually fining them an exit door. Listening to Ed Kane describe the process with BodyBio Liquid Minerals is not only interesting, but seems the only safe and healthy way to get the job done.
BodyBio Video Library - Trace Minerals Video Part One
http://www.bodybio.com/content.aspx?page=BodyBioWellnessVideoLibrary
Molecular interactions with mercury in the kidney
http://www.ncbi.nlm.nih.gov/pubmed/10699157
Mercury poisoning Wiki
http://en.wikipedia.org/wiki/Mercury_poisoning
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Improve Mitochondrial Function (CFS) crossover study:
"In a subsequent cross-over study the effects of LRT on fatigue and mitochondrial function
were monitored in patients with moderate to severe chronic fatigue. There was good
correspondence between reductions in fatigue and gains in mitochondrial function. After 8
weeks of LRT with NTFactor, mitochondrial function was significantly improved, and after 12
weeks of NTFactor supplementation, fatigue was decreased by 35.5% (p<0.001), and
mitochondrial function was found to be similar to that found in young healthy adults (26.8%
increase, p<0.0001). After 12 weeks of supplement use, subjects were placed on placebo
for an additional 12 weeks, and their fatigue and mitochondrial function were again measured.
After the placebo period, fatigue and mitochondrial function were intermediate between the
initial values and those found after 8 or 12 weeks on the supplement, indicating that continued
supplementation is required to show improvements in mitochondrial function and maintain lower
fatigue scores."
Nicolson 2014 - Use of Natural Supplements to Improve Mitochondrial Function (CFS)
http://functionalfoodscenter.net/files/81845995.pdf
CFS - The Central Cause: Mitochondrial Failure
http://drmyhill.co.uk/wiki/CFS_-_The_Central_Cause:_Mitochondrial_Failure
Dr.Myhill,
"I think this is one of the most important handouts I have ever produced in terms of my understanding of CFS and what to do in order to recover! So please read this very carefully and several times over because for many sufferers it contains the keys to unlock their illness!"
Toxic Problems: Pollution and Poisonings
http://drmyhill.co.uk/wiki/Category:Toxic_Problems:_Pollution_and_Poisonings
"In a subsequent cross-over study the effects of LRT on fatigue and mitochondrial function
were monitored in patients with moderate to severe chronic fatigue. There was good
correspondence between reductions in fatigue and gains in mitochondrial function. After 8
weeks of LRT with NTFactor, mitochondrial function was significantly improved, and after 12
weeks of NTFactor supplementation, fatigue was decreased by 35.5% (p<0.001), and
mitochondrial function was found to be similar to that found in young healthy adults (26.8%
increase, p<0.0001). After 12 weeks of supplement use, subjects were placed on placebo
for an additional 12 weeks, and their fatigue and mitochondrial function were again measured.
After the placebo period, fatigue and mitochondrial function were intermediate between the
initial values and those found after 8 or 12 weeks on the supplement, indicating that continued
supplementation is required to show improvements in mitochondrial function and maintain lower
fatigue scores."
Nicolson 2014 - Use of Natural Supplements to Improve Mitochondrial Function (CFS)
http://functionalfoodscenter.net/files/81845995.pdf
CFS - The Central Cause: Mitochondrial Failure
http://drmyhill.co.uk/wiki/CFS_-_The_Central_Cause:_Mitochondrial_Failure
Dr.Myhill,
"I think this is one of the most important handouts I have ever produced in terms of my understanding of CFS and what to do in order to recover! So please read this very carefully and several times over because for many sufferers it contains the keys to unlock their illness!"
Toxic Problems: Pollution and Poisonings
http://drmyhill.co.uk/wiki/Category:Toxic_Problems:_Pollution_and_Poisonings
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Radio, l was admitted into hospital with mercury poisoning at five months of age - Pinks Disease, and then played with it at age 9 or thereabouts with lifelong health problems but my kidneys seem to be okay. Urine sulphate is low so do you know what that implies?
adreno
PR activist
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- 4,841
Can't we just eat more sulfur foods?
Rand56
Senior Member
- Messages
- 675
- Location
- Myrtle Beach, SC
hi Adreno
I don't know if this totally answers your question in the context of what's been said above, but to provide some more information, according to Dr. Seneff, the best sulfur containing foods to eat are eggs, garlic, onion, and cruciferous veggies. She says the sulfur in those foods are easily sulfated.
As far as the supplement MSM, even though she suspects its probably metabozied to sulfate, she has yet to figure out the biochemistry that it does.
She is a big proponent of eating eggs because you also get your cholesterol from them along with the sulfur. One of the reasons why she says sun exposure is very important is because the skin synthesizes cholesterol sulfate, and cholesterol sulfate is water soluble making it more easily transported within the body.
From the podcasts and youtube's I've watched of her, I did not hear the topic being talked about of sulfur sensitivity with some people. I am not one of those but I know there are a number of people on here that are.
Rand56
Senior Member
- Messages
- 675
- Location
- Myrtle Beach, SC
Also, in one of the youtube video's I watched of Dr. Seneff, she showed a chart of the depleted minerals in the soil as a consequence of the gyphosates in the RoundUp sprayed on GMO crops. All minerals were depleted but sulfur was depleted the most.
Hey Brenda,
Sulphur is so critical to life that the body will borrow protein from the muscles to keep from running to low. Many systems in the body will not function well in a low sulphate environment. The enzyme involved is phenol sulfur-transferase (PST), needs sulfates. Low levels of sulphate can lead to retention of toxins in the body. B6 in the form of P5P inhibits PST activity. This could be why some people in this forum show adverse effects (Neuropathy), when supplements with P5P.
If you're experiencing a worsening in symptoms when taking aspirin/ibuprofen....salicylates would be the first thing to look into. Many foods are high in salicylate....especially herbs, spices, fruits and veggies. If you find that your symptoms worsen when eating the foods that contain high amounts of salicylate...it could be that your PST/sulfation is weak.
PST = phenolsulphotransferase. Its an enzyme which is involved in sulfation.....one of the body's key detoxification pathways.
The PST sulfation pathway is necessary for the breakdown and removal of certain toxins in the body. This includes the processing of a type of chemical called a phenol. Phenols are a regular and necessary part of life. All foods contain some phenolic compounds. However, some foods have a much higher content than others do. If the sulfation pathway is not functioning well, a person may not be able to process out the phenolic compounds as fast as they consume them. There is a cumulative effect. When the phenols start backing up in the system, it can cause many negative reactions
The main reason for low functioning PST is low sulfate in the body. Sulfate is essential to keep PST functioning....Sulfate is also necessary in maintaing the integrity of the intestinal lining. Low sulfate levels = increased intestinal permeability (leaky gut).
Can't we just eat more sulfur foods?
If in fact there is a high mercury load in the kidneys and sulfate wasting or possibly sulfate transport problem is occurring in some people with CFS/ME. Eating more eggs will not fix this problem. I am now considering sulfate supplementation. Also, Magnesium sulfate therapy can be problematic, When there is a sodium/potassium pump mast cell problem, that can be a contributing factor in acquired mitochondrial damage. We need to repair the mitochondria lipid bilayer and try to get sulfates in balance with out overloading the system.
Phenol Diet
http://www.healthinducedautism.com/low-phenol-diet-information.html
Foods contain salicylates
http://salicylatesen...ity.com/about#
No Sulfites Help for Food Allergy
http://www.learningtarget.com/nosulfites/
Foods high in sulfur (thiols)
http://www.livingnetwork.co.za/chelationnetwork/food/high-sulfur-sulphur-food-list/
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@Radio
Thanks. You are right about salicylates and I have s adjucts on my genes and have cut back with diet and topical. The thing I do not understand is why I am low in urine sulphate , so it is not due to sulphate wasting where urine levels would be high like with children with autism. I am doing magnesium sulphate foot baths atm and think that it helps. Thanks for the links and the explanation about p5p.
Thanks. You are right about salicylates and I have s adjucts on my genes and have cut back with diet and topical. The thing I do not understand is why I am low in urine sulphate , so it is not due to sulphate wasting where urine levels would be high like with children with autism. I am doing magnesium sulphate foot baths atm and think that it helps. Thanks for the links and the explanation about p5p.
RichVank
"The sulfate transporters in the kidneys can be blocked by mercury or other toxic metals, which build up because of glutathione depletion, and thus not enough sulfate is retained to do several important jobs, including sulfating DHEA, sulfating a range of toxins as part of Phase II detoxication, including phenols from certain foods, and supporting the cartilage in the joints. "
What else can affect this sulfates homeostasis?
Functional SUOX (B-12) Deficiency, Molybdenum Deficiency as well as possibly lacking the vitamin D receptor (VDR), NaSi-1 expression in the kidneys...Vitamin D and thyroid hormone T 3 are needed for sulfate transport.
I think DHEA-S could be a good way to test for sulfates levels in the body...
Hydrogen sulfide <-- can be a problem as well...
The gas is produced from cysteine by the enzymes cystathionine beta-synthase and cystathionine gamma-lyase. It acts as a relaxant of smooth muscle and as a vasodilator. Eventually the gas is converted to sulfite in the mitochondria by thiosulfate reductase, and the sulfite is further oxidized to thiosulfate and sulfate by sulfite oxidase.
The Infamous Hydrogen Sulfide (H2S)When gut bacteria or fungi are attacked by something like a heavy metal molecule (e.g. mercury), they have a special defense mechanism (called a "resistance gene") that produces Hydrogen Sulfide (H2S) gas, which binds to the attacker and neutralizes it. Subsequently this highly toxic and poisonous H2S gas is created in the gut. H2S can impair the immunity system, especially in the area of neutrophil function, which is used to fight the original yeast in the gut, and hence one can hit a vicious cycle. H2S is very similar to mercury, in that it can bind to many of the things that mercury binds to and inactivate them. In other words, all the bad things that mercury can do, as described here, H2S can do. H2S can also convert the safer Inorganic mercury to the more dangerous Organic mercury, as described here. H2S has a very special circular relationship with the heavy metals; and therefore, it is a very special gas.
Foods That Discourage Fermentation (good)
The following foods are helpful when one has a fermentation problem: Complex carbohydrates (e.g. brown rice, buckwheat, popcorn, rice cakes), vegetables, cranberries and blueberries (non-sweet fruit), Lingonberries (red sour small berries), no sugar soy milk, Aloe Juice, no sugar yogurt, goat yogurt, Keifer milk, cheese, milk, tomatoes, peppers, sesame-seed paste, pocono buckwheat, hominy grits (white corn grits), squashes are excellent, olives (black and green, not from metal can, w/o sulfite preservative), goat feta cheese is excellent (not cow feta), potatoes in small quantities, brown rice is excellent, millet is ok most of the time, small amounts of turkey (possibly with digestive aids), fish, flax oil, olive and weight-lifters MCT oils (caprylate + gammalinolenate), and Rutabagas (good against Candida). One can use Alanine or Stevia for sweeteners.
Healing The Gut <---(Read this)
http://www.beatcfsandfms.org/html/HealYourGut.html
Transcriptional regulation of the sodium-sulfate cotransporter NaS(i)-1 gene
http://www.ncbi.nlm.nih.gov/pubmed/12139403
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Sulfate transporters
All cells require inorganic sulfate for normal function. Sulfate is among the most important macronutrients in cells and is the fourth most abundant anion in human plasma (300 microM). Sulfate is the major sulfur source in many organisms, and because it is a hydrophilic anion that cannot passively cross the lipid bilayer of cell membranes, all cells require a mechanism for sulfate influx and efflux to ensure an optimal supply of sulfate in the body. The class of proteins involved in moving sulfate into or out of cells is called sulfate transporters. To date, numerous sulfate transporters have been identified in tissues and cells from many origins. These include the renal sulfate transporters NaSi-1 and sat-1, the ubiquitously expressed diastrophic dysplasia sulfate transporter DTDST, the intestinal sulfate transporter DRA that is linked to congenital chloride diarrhea, and the erythrocyte anion exchanger AE1. These transporters have only been isolated in the last 10-15 years, and their physiological roles and contributions to body sulfate homeostasis are just now beginning to be determined.
http://www.ncbi.nlm.nih.gov/pubmed/11581495
All cells require inorganic sulfate for normal function. Sulfate is among the most important macronutrients in cells and is the fourth most abundant anion in human plasma (300 microM). Sulfate is the major sulfur source in many organisms, and because it is a hydrophilic anion that cannot passively cross the lipid bilayer of cell membranes, all cells require a mechanism for sulfate influx and efflux to ensure an optimal supply of sulfate in the body. The class of proteins involved in moving sulfate into or out of cells is called sulfate transporters. To date, numerous sulfate transporters have been identified in tissues and cells from many origins. These include the renal sulfate transporters NaSi-1 and sat-1, the ubiquitously expressed diastrophic dysplasia sulfate transporter DTDST, the intestinal sulfate transporter DRA that is linked to congenital chloride diarrhea, and the erythrocyte anion exchanger AE1. These transporters have only been isolated in the last 10-15 years, and their physiological roles and contributions to body sulfate homeostasis are just now beginning to be determined.
http://www.ncbi.nlm.nih.gov/pubmed/11581495
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Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D3.
As the fourth most abundant anion in the body, sulfate plays an essential role in numerous physiological processes. One key protein involved in transcellular transport of sulfate is the sodium-sulfate cotransporter NaSi-1, and previous studies suggest that vitamin D modulates sulfate homeostasis by regulating NaSi-1 expression. In the present study, we found that, in mice lacking the vitamin D receptor (VDR), NaSi-1 expression in the kidney was reduced by 72% but intestinal NaSi-1 levels remained unchanged. In connection with these findings, urinary sulfate excretion was increased by 42% whereas serum sulfate concentration was reduced by 50% in VDR knockout mice. Moreover, levels of hepatic glutathione and skeletal sulfated proteoglycans were also reduced by 18 and 45%, respectively, in the mutant mice. Similar results were observed in VDR knockout mice after their blood ionized calcium levels and rachitic bone phenotype were normalized by dietary means, indicating that vitamin D regulation of NaSi-1 expression and sulfate metabolism is independent of its role in calcium metabolism. Treatment of wild-type mice with 1,25-dihydroxyvitamin D3 or vitamin D analog markedly stimulated renal NaSi-1 mRNA expression. These data provide strong in vivo evidence that vitamin D plays a critical role in sulfate homeostasis. However, the observation that serum sulfate and skeletal proteoglycan levels in normocalcemic VDR knockout mice remained low in the absence of rickets and osteomalacia suggests that the contribution of sulfate deficiency to development of rickets and osteomalacia is minimal.
Tubular handling and regulation of sulphate
http://ndt.oxfordjournals.org/content/15/suppl_6/34.full.pdf
Critical role of vitamin D in sulfate homeostasis:
http://www.ncbi.nlm.nih.gov/pubmed/15165995
As the fourth most abundant anion in the body, sulfate plays an essential role in numerous physiological processes. One key protein involved in transcellular transport of sulfate is the sodium-sulfate cotransporter NaSi-1, and previous studies suggest that vitamin D modulates sulfate homeostasis by regulating NaSi-1 expression. In the present study, we found that, in mice lacking the vitamin D receptor (VDR), NaSi-1 expression in the kidney was reduced by 72% but intestinal NaSi-1 levels remained unchanged. In connection with these findings, urinary sulfate excretion was increased by 42% whereas serum sulfate concentration was reduced by 50% in VDR knockout mice. Moreover, levels of hepatic glutathione and skeletal sulfated proteoglycans were also reduced by 18 and 45%, respectively, in the mutant mice. Similar results were observed in VDR knockout mice after their blood ionized calcium levels and rachitic bone phenotype were normalized by dietary means, indicating that vitamin D regulation of NaSi-1 expression and sulfate metabolism is independent of its role in calcium metabolism. Treatment of wild-type mice with 1,25-dihydroxyvitamin D3 or vitamin D analog markedly stimulated renal NaSi-1 mRNA expression. These data provide strong in vivo evidence that vitamin D plays a critical role in sulfate homeostasis. However, the observation that serum sulfate and skeletal proteoglycan levels in normocalcemic VDR knockout mice remained low in the absence of rickets and osteomalacia suggests that the contribution of sulfate deficiency to development of rickets and osteomalacia is minimal.
Tubular handling and regulation of sulphate
http://ndt.oxfordjournals.org/content/15/suppl_6/34.full.pdf
Critical role of vitamin D in sulfate homeostasis:
http://www.ncbi.nlm.nih.gov/pubmed/15165995
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Bypassing the sulfate deficiency? D-Glucosamine Sulfate and Chondroitin Sulfate 24/7 Topical Patches?
• Skin patches bypass the digestive system
• Provides a steady delivery directly to the bloodstream
• Helps with joint problems, such as joint pain, stiffness, and inflammation.
www.amazon.com/dp/B00G4EBZAU/ref=wl_it_dp_o_pC_nS_ttl?_encoding=UTF8&colid=STE6K5DNMJYK&coliid=I1FBIUO21DV2A4
Enzymatic Therapy, Better Veins ?
Glycosaminoglycans (GAGs) are a mixture of highly purified compounds such as dermatan sulfate, heparan sulfate, hyaluronic acid, chondroitin sulfate, and related hexosaminoglycans.
http://www.iherb.com/Enzymatic-Ther...ic Therapy - Better Veins&rc=148&sr=null&ic=1
• Skin patches bypass the digestive system
• Provides a steady delivery directly to the bloodstream
• Helps with joint problems, such as joint pain, stiffness, and inflammation.
www.amazon.com/dp/B00G4EBZAU/ref=wl_it_dp_o_pC_nS_ttl?_encoding=UTF8&colid=STE6K5DNMJYK&coliid=I1FBIUO21DV2A4
Enzymatic Therapy, Better Veins ?
Glycosaminoglycans (GAGs) are a mixture of highly purified compounds such as dermatan sulfate, heparan sulfate, hyaluronic acid, chondroitin sulfate, and related hexosaminoglycans.
http://www.iherb.com/Enzymatic-Ther...ic Therapy - Better Veins&rc=148&sr=null&ic=1
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Reverse-Mitochondrial-Damage-101
http://forums.phoenixrising.me/index.php?threads/reverse-mitochondrial-damage-101.28175/
http://forums.phoenixrising.me/index.php?threads/reverse-mitochondrial-damage-101.28175/
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