A Relationship Between Vitamin B₁₂, Folate, Ascorbic Acid, and Mercury Metabolism

The effect of megadoses of vitamin B₁₂, folate, and vitamin C on the in vivo methylation of mercuric chloride was studied in guinea pigs. The incorporation of high levels of vitamin B₁₂, folate, and vitamin C resulted in a decrease in both inorganic mercury and methylmercury concentrations in all tissues except the lung and heart compared to controls. However, percent methylmercury levels tended to increase with vitamin treatments.

The addition of megadoses of vitamin B₁₂ fed either singularly or in combination with the other vitamins resulted in increased methylmercury concentrations in the liver, spleen, and kidney tissues of the guinea pig. Moreover, percent methylmercury levels increased with B₁₂ treatment in the liver, heart, and kidney. Incorporation of high levels of folate into the dietary regime also affected the mercury methylation process particularly in the liver, heart, kidney and hair tissues. However, this effect was observed most often in animals fed both B₁₂ and folate. Vitamin C appears to play a synergistic role with vitamin B₁₂ and/or folate in the methylation of mercury.

Auditory brainstem responses (ABR) produced results which supported the theory that vitamin B₁₂ treatment can potentiate the mercury effect in the auditory pathways of the guinea pig. Wave latencies were longer and threshold values were higher in animals fed megadoses of B₁₂. Interpeak latency means were also longer in animals treated with vitamins and mercury compared to untreated controls.

Rats fed diets supplemented with either methionine or cysteine exhibited differences in methylmercury levels. Both methionine and cysteine supplementation resulted in a significant increase in percent methylmercury levels in the liver and kidney.

These data indicate that megadoses of vitamin B₁₂, folate, and/or vitamin C may alter the methylation process of mercury in vivo. In addition, methionine or cysteine supplementation can effect the metabolism of mercuric chloride possibly via transmethylation processes.