I'll comment on some of your detox ones as I have some the same so will cut and past the basic info I put together from a couple of sites on the ones I have as well. (this info below is a blend of info I cut and pasted from places with more complicated pieces left out, so I cant precisely reference it except mostly genetic genie info).
SOD2
Superoxide dismutase 2, mitochondrial
also known as
SOD2, is an
enzyme which in humans is encoded by the
SOD2 gene.
This gene is a member of the iron/manganese
superoxide dismutase family. It encodes a mitochondrial matrix protein that forms a homotetramer and binds one manganese ion per subunit. This protein transforms toxic
superoxide, a byproduct of the
mitochondrial electron transport chain, into
hydrogen peroxide and diatomic
oxygen.
Mutations in this gene have been associated with
idiopathiccardiomyopathy (IDC), sporadic motor neuron disease, and cancer. Mice lacking Sod2 die shortly after birth, indicating that unchecked levels of superoxide are incompatible with mammalian life.
[3] However, mice 50% deficient in Sod2 have a normal lifespan and minimal phenotypic defects but do suffer increased DNA damage and increased incidence of cancer.
[4]
................
NAT2
N-acetyltransferase 2 (arylamine N-acetyltransferase)
is an
enzyme which in humans is encoded by the
NAT2 gene.
[1]
This gene encodes a type of
N-acetyltransferase. The NAT2
isozyme functions to both activate and deactivate arylamine and
hydrazine drugs and carcinogens. Polymorphisms in this gene are responsible for the N-acetylation polymorphism in which human populations segregate into rapid, intermediate, and slow
acetylator phenotypes. Polymorphisms in NAT2 are also associated with higher incidences of cancer and drug toxicity. A second arylamine N-acetyltransferase gene (NAT1) is located near NAT2.
[2]
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GSTP1
Glutathione S-transferase P
is an
enzyme that in humans is encoded by the
GSTP1 gene.
[1]HYPERLINK \l "cite_note-pmid7587384-2"[2]
Glutathione S-transferases (GSTs) are a family of enzymes that play an important role in detoxification by catalyzing the conjugation of many
hydrophobic and electrophilic compounds with reduced
glutathione. Based on their biochemical, immunologic, and structural properties, the soluble GSTs are categorized into 4 main classes: alpha, mu, pi, and theta. The glutathione S-transferase pi gene (GSTP1) is a polymorphic gene encoding active, functionally different GSTP1 variant proteins that are thought to function in
xenobiotic metabolism and play a role in susceptibility to
cancer, and other diseases.
[3]
(note.. many pharma drugs are xenobiotic kind of drugs.. over 25% of pharma drugs are)
...........
CYP1B1
Cytochrome P450 1B1
is an
enzyme that in humans is encoded by the
CYP1B1 gene.
CYP1B1 belongs to the
cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. The enzyme encoded by this gene localizes to the endoplasmic reticulum (
ER) and metabolizes procarcinogens such as polycyclic aromatic hydrocarbons and 17beta-estradiol.
CYP1B1 was not identified and sequenced until 1994. Recently CYP1B1 has been shown to be physiologically important in fetal development, since mutations in CYP1B1 are linked with a form of primary congenital glaucoma. It is thought that the enzyme also metabolizes a signaling molecule involved in eye development, possibly a steroid.
CYP1B1 is regulated by the
Aryl hydrocarbon receptor, a ligand activated transcription factor. It is part of the Phase I reactions in
drug metabolism.
.......................
CYP2D6
Cytochrome P450 2D6
is an
enzyme that in humans is encoded by the
CYP2D6 gene. CYP2D6 is primarily expressed in the liver.
CYP2D6 a member of the
cytochrome P450 mixed-function oxidase system, is one of the most important enzymes involved in the
metabolism of
xenobiotics in the body. In particular, CYP2D6 is responsible for the metabolism and
elimination of approximately 25% of clinically used drugs.
[1] This enzyme also metabolizes several endogenous substances such as
hydroxytryptamines and
neurosteroids.
[1]
There is considerable variation in the efficiency and amount of CYP2D6 enzyme produced between individuals. Hence for drugs that are metabolized by CYP2D6 (that is are CYP2D6
substrates), certain individuals will eliminate these drugs quickly (extensive metabolizers) while others slowly (poor metabolizers). If a drug is metabolized too quickly, it may decrease the drug's
efficacy while if the drug is metabolized too slowly, toxicity may result.
[2] Hence the dose of the drug may have to be adjusted to take into account of the speed at which it is metabolized by CYP2D6.
[3]
In addition, other drugs may function as
inhibitors of CYP2D6 activity or
inducers of CYP2D6 enzyme expression that will lead to decreased or increased CYP2D6 activity respectively. If such a drug is taken at the same time a second drug who is a CYP2D6 substrate, the first drug may affect the elimination rate of the second through what is known as a
drug-drug interaction.
[2]
CYP2D6 shows the largest
phenotypical variability among the CYPs, largely due to
genetic polymorphism. The
genotype accounts for normal, reduced, and non-existent CYP2D6 function in subjects.
The CYP2D6 function in any particular subject may be described as one of the following:
[5]
poor metabolizer – little or no CYP2D6 function
intermediate metabolizers – metabolize drugs at a rate somewhere between the poor and extensive metabolizers
extensive metabolizer – normal CYP2D6 function
ultrarapid metabolizer – multiple copies of the
CYP2D6 gene are expressed, and therefore greater-than-normal CYP2D6 function
........
Be aware that the ordinary wikipedia has some info the the various gene families too if you put in something like CYP2D6 etc. .
www.genecards.org is a good place to look for info on various genes.
