Vitamin interaction with zinc

In the diet and at the tissue level, ascorbic acid can interact with mineral nutrients. In the intestine, ascorbic acid enhances the absorption of dietary iron and selenium reduces the absorption of copper, nickel, and manganese but apparently has little effect on zinc or cobalt. Ascorbic acid fails to affect the intestinal absorption of two toxic minerals studied, cadmium and mercury. At the tissue level, iron overload enhances the oxidative catabolism of ascorbic acid. Thus, the level of dietary vitamin C can have important nutritional consequences through a wide range of inhibitory and enhancing interactions with mineral nutrients. 

Clinically important, potentially hazardous interactions with acitretin, aluminum salts, amoxicillin, ampicillin, antacids, bacampicillin, bismuth, calcium, carbenicillin, cloxacillin, digoxin, iron salts, isotretinoin, magnesium salts, methotrexate, methoxyflurane, mezlocillin, nafcillin, oxacillin, penicillins, piperacillin, ticarcillin, vitamin A, zinc, zinc salts... 

Among humans, abnormal dark adaptation is reported in both vitamin A deficiency and zinc deficiency and is especially prevalent in alcoholic cirrhotics (Patek and Haig, 1939 Russell et aL, 1973 Morrison et aL, 1978 McClain et aL, 1979). In the former but not in the latter deficiency, treatment with vitamin A reverses the abnormality (Russell et aL, 1978) only after correcting the zinc deficiency does dark adaptation become normal in the latter case (Morrison et aL, 1978 McClain et aL, 1979). The molecular basis for these observations may be associated, at least in part, with the activity of retinaldehyde reductase in the retina which, as already mentioned, Huber and Gershoff (1975) showed to be especially sensitive to the level of zinc nutriture and Mezey and Holt (1971) showed was competitively inhibited by the presence of ethanol. In the alcoholic cirrhotic, however, the zinc-vitamin A interaction may be further complicated by a defective hepatic synthesis of transport proteins (Mobarhan et aL, 1981) or failure to sequester or retain zinc Nutrition Reviews, 1982) and/or vitamin A (Sato and Lieber, 1981 Leo and Lieber, 1982) in the appropriate tissues. The implications for human nutrition of the interaction of vitamin A and zinc were reviewed by Solomons and Russell (1980). 

Relationships between plasma vitamin A and zinc were explored in 45 children with clinical vitamin A deficiency and 20 children with PEM (Shingwekar et al., 1979). Mean levels of plasma vitamin A, RBP, and zinc were low in these malnourished children compared to controls. Supplementation with zinc resulted in a small but significant increase in plasma vitamin A and RBP levels in children with PEM but not in the vitamin A-deficient group. There was no correlation between plasma levels of vitamin A and zinc. It was suggested that in children with PEM, apart from deficiencies of protein and vitamin A, zinc deficiency may also contribute in part to low plasma vitamin A levels. Other clinical studies on the interaction between zinc and vitamin A are discussed in the above-mentioned reviews. Zinc deficiency is an uncommon but potential contributor to abnormal vitamin A transport in a number of gastrointestinal and hepatic diseases, as well as in PEM. 

Zinc is the prosthetic group of more than a hundred enzymes with a wide variety of functions. It is also involved in the receptor proteins for steroid and thyroid hormones, calcitriol and vitamin A. In these proteins, zinc forms an integral part of the region of the protein that interacts with the promoter site on DNA to initiate gene transcription in response to hormone action (section 10.4). 

INTERRELATIONSHIPS. Manganese interacts with other nutrients. Excess calcium and phosphorus interfere with the absorption of manganese the functions of manganese, copper, zinc, and iron may be interchangeable in certain enzyme systems and manganese and vitamin K work together in the promotion of blood clotting. 

Thawley DG, Willoughby RA, McSherry BJ. et al. 1977. Toxic interaction among lead, zinc, and cadmium with varying levels of dietary calcium and vitamin D. Environ Res 14 463-475. 

The main action of vitamin E in human tissue is to prevent oxidation of polyunsaturated fatty acids (PUFA), thereby protecting lipid and phospholipids in membranes. Vitamin E interacts syn-ergically with other nutrients, such as vitamin C, selenium, and zinc, which are also involved in the oxidation pathway. The recommended intake is strongly related to the quantity of PUFA consumption. Some studies [454-456] on animal models and epidemiological trials in human suggest... 

Warfarin The exact warfarin-quinolone drug interaction is unknown. Reduction of intestinal flora responsible for vitamin K production by antibiotics is probable, as are deaeased metabolism and clearance of warfarin due to CYP450 inhibition by the quinolones. Multivalent cations such as aluminum, magnesium, calcium, iron, zinc, and multivitamins with minerals may chelate with fluoroquinolones and decease the oral absorption if administered concurrently. 

There are numerous reports of interactions of dietary elements that cause variation in the absorption of chromium. Amino acids, which chelate chromium, prevent precipitation at the basic pH in the small intestine, which increases its absorption [13]. Other chelating agents have mixed effects. Phytates significantly decrease absorption whereas oxalates lead to increased absorption [15]. Certain vitamins such as nicotinic acid and ascorbic acid have been shown to increase absorption [16]. Starch has also been shown to increase absorption to a greater degree than glucose, fructose, and sucrose. Some metals can compete with chromium and decrease its absorption. Studies show that zinc, vanadium, and iron have a common intestinal transport mechanism with chromium and can decrease the absorption of chromium [9]. 

---