Vitamin A is involved in zinc metabolism and vice versa. So zinc can have an effect on Vitamin A function. Ceruloplasmin needed to make our copper and iron bioavailable (usable) is dependent on zinc and Vitamin A as well. For example from the research, Zinc deficiency is thought to interfere with vitamin A metabolism in several ways: (1) Zinc deficiency results in decreased synthesis of retinol-binding protein (RBP), which transports retinol through the circulation to peripheral tissues for its utilization by the body and protects the organism against potential toxicity of retinol; (2) zinc deficiency results in decreased activity of the enzyme that releases retinol from its storage form, retinyl palmitate, in the liver; and (3) zinc is required for the enzyme that converts retinol into retinal. Zinc is involved in that conversion of retinol to retinaldehyde (retinal) and retinal to retinoic acid, respectively - The zinc metalloenzyme ADH is required for this oxidative process.
Zinc uptake/absorption is lowered and also becomes less available to utilize during chronic inflammation/infection when pro inflammatory cytokines are present since zinc is being sequestered into the cell and therefore is a central problem for all chronic inflammatory conditions.
Vitamin A also has antioxidant properties. Immunity is also compromised upon loss of Vitamin A. Vitamin A insufficiency is associated with increased mortality to lung infections and immune responses to infection were compromised upon loss of Vitamin A, and that Retinoic Acid served to activate the T cells driving these responses.
https://www.medicalnewstoday.com/articles/219513#1
Retinoid X receptor (RXR) requires Vitamin A. The RXR also forms a heterodimer with a number of other receptors (e.g., vitamin D and thyroid hormone). Vitamin A is crucial in activating Retinoid X Receptors (RXR), which is also required for PPAR activation. All PPARs heterodimerize with the retinoid X receptor (RXR) and bind to specific regions on the DNA of target genes Zinc is involved in Vitamin A metabolism and vice versa. https://pubmed.ncbi.nlm.nih.gov/23440512/
Zinc and Vitamin A are both lowered from inflammation and infection, especially with fever.
Episodes of acute infection deplete body stores of vitamin A. We have found that significant amounts of retinol and retinol-binding protein (RBP) were excreted in the urine during serious infections, whereas only trace amounts were found in the urine of healthy control subjects. Subjects with fever (temperature > or = 38.3 degrees C) excreted significantly more retinol (geometric mean = 1.67 mumol/d) than did those without fever.
https://ajcn.nutrition.org/article/S0002-9165(23)18442-5/fulltext Severe infections in adult patients (i.e., sepsis and pneumonia) result in excretion of large quantities of Vitamin A retinol in the urine and depletion of vitamin A stores.
https://www.ncbi.nlm.nih.gov/pubmed/7762530/ https://www.cambridge.org/core/jour...h-ascariasis/AF0B9F3B859B6F96E963E488D14477BB Retinol levels decline rapidly as part of the acute phase response
https://www.sciencedirect.com/science/article/pii/S0002916523068545?via=ihub and this translates into increased susceptibility to infection, creating a “vicious circle” difficult to break
https://www.ncbi.nlm.nih.gov/pubmed/10466190/
VitA is also toxic if you take too much, so don't think "VitA is good for me, I'll take lots".
The gene encoding alcohol dehydrogenase-1 (Adh1) (which requires Zinc.) greatly facilitates degradative metabolism of excess Vitamin A retinol into retinoic acid which may help protect against toxic effects of high dietary vitamin A intake or supplementation. and also helps convert to the active forms.
https://portlandpress.com/biochemj/...lular-retinol-binding?redirectedFrom=fulltext
Since there are no known enzymes that can reduce retinoic acid to retinal, excessive or unneeded retinoic acid is not recycled back to retinol/retinyl ester and must be catabolized and eliminated from the body. This catabolism is catalyzed by one of several cytochrome P450 (CYP) enzymes which require magnesium. Any factor that lowers magnesium or cytochrome P450 enzymes can lead to excessive retinoic acid.
https://www.jlr.org/article/S0022-2275(20)42124-8/fulltext
Over 600 enzyme systems require Magnesium as a cofactor to function optimally, including the cytochrome P450 enzymes (CYP450
https://www.liebertpub.com/doi/abs/10.1089/pai.1994.8.7
Some more:
https://forums.phoenixrising.me/threads/dang-those-vitamin-d3-levels.91152/post-2450587