Abstract
Degradation 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\((O_{2^ - } )\) 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\(O_{2^ - } \) and H2O2, might be the oxygen free radical mainly responsible for the degradation of MeHg and EtHg.
Similar content being viewed by others
Abbreviations
- Hg:
-
mercury
- MeHg:
-
methyl mercury
- EtHg:
-
ethyl mercury
- \(O_{2^ - } \) :
-
Superoxide anion
- H2O2 :
-
hydrogen peroxide
- •OH:
-
hydroxyl radical
- 1O2 :
-
singlet oxygen
- HOCl:
-
hypochlorous acid
- NAC:
-
N-acetyl-l-cysteine
- XOD:
-
xanthine oxidase
- HPX:
-
hypoxanthine
- Fe(III)EDTA:
-
ferric monosodium ethylenediaminetetraacetate
- DETAPAC:
-
diethylenetriamine pentaacetic acid
- SOD:
-
Superoxide dismutase
- UV:
-
ultraviolet light
References
Czapski G (1984) Reaction of •OH. In: Methods in enzymology, vol 105 Academic Press, Inc., New York, pp 209–215
Freeman BA, Crapo JD (1982) Biology of disease: free radicals and tissue injury. Lab Invest 47: 412–426
Gage JC (1975) Mechanisms for the biodegradation of organic mercury compounds: the actions of ascorbate and of soluble proteins. Toxicol Appl Pharmacol 32: 225–238
Ganther HE (1980) Interactions of vitamin E and selenium with mercury and silver. Ann N Y Acad Sci 355: 212–226
Godfrey RW, Wilder MS (1984) Relationships between oxidative metabolism, macrophage activation, and antilisterial activity. J Leukoc Biol 36: 533–543
Halliwell B, Gutteridge JMC (1981) Formation of a thiobarbituric-acid reactive substance from deoxyribose in the presence of iron salts: the role of Superoxide and hydroxyl radicals. FEBS Lett 128: 347–352
Halliwell B, Gutteridge JMC (1984) Oxygen toxicity, oxygen radicals. transition metals and disease. Biochem J 219: 1–14
Harbour JR, Chow V, Bolton JR (1974) An electron spin resonance study of the spin adducts of OH and HO2 radicals with nitrones in the ultraviolet photolysis of aqueous hydrogen peroxide solutions. Can J Chem 52: 3549–3553
Klebanoff SJ (1980) Oxygen metabolism and the toxic properties of phagocytes. Ann Int Med 93: 480–489
Konishi T, Takahashi H (1983) Direct determination of inorganic mercury in biological materials after alkali digestion and amalgamation. Analyst 108: 827–834
Magos L, Brown AW, Sparrow S, Bailey E, Snowden RT, Skipp WR (1985) The comparative toxicology of ethyl- and methylmercury. Arch Toxicol 57: 260–267
Norseth T (1971) Biotransformation of methyl mercuric salts in germ free rats. Acta Pharmacol Toxicol 30: 172–176
Norseth T, Clarkson TW (1970) Studies on the biotransformation of203Hg-labeled methyl mercury chloride in rats. Arch Environ Health 21: 717–727
Parker CW (1984) Mediators: Release and function. In: Paul WE (ed) Fundamental immunology. Raven Press, New York, pp 697–747
Pick E, Keisari Y (1980) A simple colorimetric method for the measurement of hydrogen peroxide produced by cells in culture. J Immunol Methods 38: 161–170
Rowland IR, Davies MJ, Evans JG (1980) Tissue content of mercury in rats given methylmercuric chloride orally: influence of intestinal flora. Arch Environ Health 35: 155–160
Rowland IR, Robinson RD, Doherty RA (1984) Effects of diet on mercury metabolism and excretion in mice given methylmercury: role of gut flora. Arch Environ Health 39: 401–408
Rowley DA, Halliwell B (1983) Superoxide-dependent and ascorbate-dependent formation of hydroxyl radicals in the presence of copper salts: a physiologically significant reaction? Arch Biochem Biophys 225: 279–284
Suda I, Takahashi H (1986) Enhanced and inhibited biotransformation of methyl mercury in the rat spleen. Toxicol Appl Pharmacol 82: 45–52
Suda I, Takahashi H (1990) Effect of reticuloendothelial blockade on the biotransformation of methyl mercury in the rat. Bull Environ Contam Toxicol 44: 609–615
Takahashi H, Suda I (1986) Metabolic fate of methylmercury in animals. In: Tsubaki T, Takahashi H (eds) Recent advances in Minamata disease studies. Kodansha, Tokyo, pp 135–150
Winterbourn CC, Stern A (1987) Human red cells scavenge extracellular hydrogen peroxide and inhibit formation of hypochlorous acid and hydroxyl radical. J Clin Invest 80: 1486–1491
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Suda, I., Totoki, S. & Takahashi, H. Degradation of methyl and ethyl mercury into inorganic mercury by oxygen free radical-producing systems: Involvement of hydroxyl radical. Arch Toxicol 65, 129–134 (1991). https://doi.org/10.1007/BF02034939
Received:
Revised:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF02034939