Dietary Strategies for the Treatment of Cadmium and Lead Toxicity - 03 Vitamins
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Nutrients. 2015 Jan; 7(1): 552–571. Published online 2014 Jan 14. doi: 10.3390/nu7010552 PMCID: PMC4303853 Dietary Strategies for the Treatment of Cadmium and Lead Toxicity - Qixiao Zhai,1 Arjan Narbad,2 and Wei Chen1,3,*
Vitamins are vital nutrients for humans and can easily be obtained from the diet. Vitamin C, B1 and B6 deficiencies have been reported to enhance sensitivity towards Cd and Pb toxicity. Vitamin supplementation has proved to be effective against Cd and Pb toxicity in both human and animal studies.
Vitamins C and E are natural non-enzymatic antioxidants that are able to scavenge free radicals and decrease lipid peroxidation. Many studies on the effects of vitamins C and E on Cd and Pb intoxication have been performed.
Vitamin C attenuates the oxidative damage and histopathological changes induced by CdCl2 in the lungs and brain of rats. It has similar protective effects in the liver, kidney, brain and the testes of Pb-exposed rats. Apart from its well-established antioxidant properties, vitamin C has been reported to act as a chelating agent of Pb, with a similar potency to that of EDTA. Probably due to this chelating capacity, a decrease of blood Pb levels from 1.8 ± 0.05 μmol/L to 0.4 ± 0.05 μmol/L (p ≤ 0.01) was observed in a study of 75 adult smokers receiving 1 g vitamin C daily for one week. However, it is noteworthy that very few animal studies can confirm the positive impact of vitamin C on reducing blood Pb levels. Indeed a human clinical study with 52 adult male subjects found that 3 months of vitamin C supplementation had no impact on the levels of Pb in blood or hair .
Pre-treatment with vitamin E exhibits protective effects against Cd toxicity, as measured by the haematological values, lipid peroxide concentration and antioxidant defence system in the blood, liver and brain of rats . The combination of vitamins C and E also resulted in reduction of oxidative stress-related damage to spermatogenesis in Cd-exposed mice and protects steroid production in Cd-exposed rats.
In a recent study of workers exposed to Pb (73 μg Pb/dL blood), after one year of oral vitamin C and E supplementation (1 g daily vitamin C and 400 IU daily vitamin E), lipid peroxidation in erythrocytes was reduced to values between 47.1% and 69.4%, which were no longer statistically different to those of the non-Pb exposed workers. The total antioxidant capacity in erythrocytes was also reversed to values between 58.9% and 67.7% in Pb-exposed workers after treatment, a level that was similar to those in non-Pb exposed workers.
Dietary vitamin B1 supplement has been reported to decrease Pb levels in the liver, kidneys, bone and blood, and recover ALAD activity in the blood in animal studies. Vitamin B1 influences the absorption of Pb and its pyrimidine ring mediates its interaction with Pb, which may cause an increase in Pb excretion and the alleviation of its toxicity.
Vitamin B6 has also been found to be effective in reducing accumulation of Pb in tissues and in reduction of inhibition of ALAD activity. This function is likely to be attributed to the ring nitrogen atom in its structure, which can chelate Pb before it is absorbed.
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