Ikuo Suda

Degradation of methyl and ethyl mercury into inorganic mercury by hydroxyl radical produced from rat liver microsomes.

Liver microsomes were prepared from Wistar rat by the Ca2+ aggregation method. Under various conditions, ethyl mercury chloride (EtHgCl) or methyl mercury chloride (MeHgCl) was incubated with the microsomal preparations. After the incubation, the amounts of inorganic Hg and hydroxyl radical (·OH) in the preparations were determined. Although the preparations alone produced a small amount of inorganic Hg and ·OH, the addition of NADPH to the preparations increased both inorganic Hg and ·OH production, which were further accelerated by the addition of KCN. The addition of Fe(III)EDTA, a ·OH formation promoter, to the microsome-NADPH-KCN system increased inorganic Hg production, whereas the addition of diethylenetriamine pentaacetic acid, a ·OH formation inhibitor, decreased inorganic Hg production. When ·OH scavengers such as mannitol and dimethyl sulfoxide were added to this system, the inorganic Hg production decreased. These results suggested that the ·OH produced from liver microsomes was responsible for the degradation of MeHg and EtHg. Since both ·OH and inorganic Hg production decreased with a concomitant decrease in NADPH-cytochrome P-450 reductase activities, it is suggested that this enzyme may be involved in the microsomal degradation of MeHg and EtHg.

A fetal type of minamata disease. An autopsy case report with special reference to the nervous system

Our knowledge concerning the pathology of fetal cases of human Minamata disease (methylmercury poisoning) is relatively limited. We report here a case with description of the distribution of mercury in the systemic organs, and the ultrastructural changes of the nervous system after a survival of 29 yr. The patient was a female born in 1957, with a body wt of 3000 g, who died in 1987. She carried a diagnosis of cerebral palsy, and had a convulsion at age 3 yr. Mercury levels in her mothers hair were 101 micrograms/g at the time of examination in 1959. At autopsy, the body measured 43 cm and weighed 23 kg. The brain weighed 920 g and showed marked cerebral atrophy, mild neuronal loss in the calcarine, postcentral and precentral cortices, cerebellar atrophy, and segmental demyelination of peripheral nerves. Mercury granules were present in the brain, kidney, and liver. Ultrastructural examination of the calcarine, post- and precentral cortices, and cerebellar cortices, showed severe atrophy of nerve cells, with a decrease in rough ER and an increase in nuclear chromatin and preservation of mitochondria. Autophagosomes were increased in number. In addition, high electron density, globular and dense bodies, measuring 0.3-1.8 microns in diameter, were found, surrounded by limited membrane, within both cerebral and cerebellar neurons. In the cellebellum, synapses were well-preserved.

Degradation of methyl and ethyl mercury into inorganic mercury by oxygen free radical-producing systems: Involvement of hydroxyl radical

AbstractDegradation of methyl mercury (MeHg) and ethyl Hg (EtHg) with oxygen free radicals was studied in vitro by using three well-known hydroxyl radical (•OH)-producing systems, namely Cu2+-ascorbate, xanthine oxidase (XOD)-hypoxanthine (HPX)-Fe(III)EDTA and hydrogen peroxide (H2O2)-ultraviolet light B. For this purpose, the direct determination method for inorganic Hg was employed. MeHg and EtHg were readily degraded by these three systems, though the amounts of inorganic Hg generated from MeHg were one half to one third those from EtHg. Degradation activity of XOD-HPX-Fe(III)EDTA system was inhibited by Superoxide dismutase, catalase and the •OH scavengers and stimulated by H2O2. Deletion of the •OH formation promoter Fe(III)EDTA from XOD-HPX-Fe(III)EDTA system resulted in the decreased degradation of MeHg and EtHg, which was enhanced by further addition of the iron chelator diethylenetriamine pentaacetic acid. In all these cases, a good correlation was observed between alkyl Hg degradation and deoxyribose oxidation determining •OH. By contrast, their degradation appeared to be unrelated to either Superoxide anion

Degradation of methyl and ethyl mercury into inorganic mercury by other reactive oxygen species besides hydroxyl radical

(O_{2^ - } )

Effect of reticuloendothelial system blockade on the biotransformation of methyl mercury in the rat

production or H2O2 production alone. We further confirmed that H2O2 (below 2 mM) itself did not cause significant degradation of MeHg and EtHg. These results suggested that •OH, but not

Involvement of Reactive Oxygens in Demethylation of Methylmercury in vivo (Proceedings of the 19th Symposium on Toxicology and Environmental Health)

O_{2^ - }