Effects of Reactive Oxygen Modulators on in vivo Demethylation of Methylmercury

Kimiko Hirayama^a and Akira Yasutake^b

^aKumamoto University College of Medical Science, 4-24-1 Kuhonji, Kumamoto 862-0976, Japan and ^bNational Institute for Minamata Disease, Minamata 867-0008, Japan

To elucidate the involvement of reactive oxygen in in vivo demethylation of methylmercury (MeHg), the effects of paraquat (PQ) and other reactive oxygen modulators on inorganic-Hg (I-Hg) production in MeHg-administered rats were examined. Rats were intravenously (i.v.) injected with MeHgCl (2 mg/kg). After MeHg administration, I-Hg levels time-dependently increased in the liver up to 9 h, whereas the renal levels did not change during the first 3 h, and then increased up to 24 h in a time-dependent manner. PQ stimulated I-Hg production in the liver but not in the kidney, whereas it increased 2-thiobarbituric acid-reactive substance (TBA-RS) levels in both tissues. PQ-induced stimulation of I-Hg production was not further accelerated by an OH・ enhancer, such as FeSO４ or Fe(III)EDTA. Hepatic I-Hg production in MeHg-administered rats (without PQ) was suppressed by NaCN (a potent inhibitor of mitochondrial cytochorome oxidase) but not by desferal or Fe(III)EDTA ( an OH・ modulalator). These results suggest that hepatic mitochondria may play an important role in in vivo demethylation of MeHg, and that reactive oxygen species other than OH・ may participate in it.