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Selenite prevents the induction of sister-chromatid exchanges by methyl mercury and mercuric chloride in human whole-blood cultures.

作者信息

Morimoto K, Iijima S, Koizumi A

出版信息

Mutat Res. 1982 Sep;102(2):183-92. doi: 10.1016/0165-1218(82)90118-5.

DOI:10.1016/0165-1218(82)90118-5
PMID:6216401
Abstract

The protective effect of sodium selenite (Na2SeO3) against the cytogenetic toxicity of methyl mercury (CH3HgCl) and mercuric chloride (HgCl2) were investigated on human whole-blood cultures in relation to induction of sister-chromatid exchange (SCE). Both mercurials caused a dose-dependent increase in SCEs, methyl mercury being about 5 times more potent than mercuric chloride. Sodium selenite also induced SCEs. However, the simultaneous addition of selenite (1 x 10(-7) -3 x 10(-5) M) to cell cultures containing either methyl mercury (3 x 10(-6) M) or mercuric chloride (1 x 10(-5) M) prevented the induction of SCEs by the mercurial in a clear dose-related manner. When selenite and mercurial were simultaneously added at a molar ratio of 1:2 Na2SeO3:CH3HgCl, or 1:1 Na2SeO3:HgCl2, cells from treated cultures showed no increase in the SCE frequency. These results indicate that selenite and mercury mutually antagonize their ability to cause DNA damage leading to the formation of SCEs. The formation of bis(methylmercuric)selenide, (CH3Hg)2Se, from Na2SeO3 and CH3HgCl, or a high molecular complex consisting of glutathione-Se-Hg from Na2SeO3 and HgCl2 involving the participation of glutathione in RBCs might play a key role in this antagonism between mercury and selenium.

摘要

相似文献

1
Selenite prevents the induction of sister-chromatid exchanges by methyl mercury and mercuric chloride in human whole-blood cultures.
Mutat Res. 1982 Sep;102(2):183-92. doi: 10.1016/0165-1218(82)90118-5.
2
Sister-chromatid exchange induction by sodium selenite: plasma protein-bound selenium is not the active SCE-inducing metabolite of Na2SeO3.
Mutat Res. 1982 Oct-Nov;102(3):285-96. doi: 10.1016/0165-1218(82)90138-0.
3
Sister-chromatid exchange induction by sodium selenite: reduced glutathione converts Na2SeO3 to its SCE-inducing form.亚硒酸钠诱导姐妹染色单体交换:还原型谷胱甘肽将Na2SeO3转化为其诱导姐妹染色单体交换的形式。
Mutat Res. 1984 Sep;141(1):49-53. doi: 10.1016/0165-7992(84)90037-x.
4
[Studies on the behavior of mercury and selenium in blood of mice injected with those elements].[关于注射汞和硒元素的小鼠血液中汞和硒行为的研究]
Hokkaido Igaku Zasshi. 1985 Mar;60(2):227-40.
5
Dependence of the sister-chromatid exchange-inducing abilities of inorganic selenium compounds on the valence state of selenium.无机硒化合物诱导姐妹染色单体交换的能力对硒价态的依赖性。
Mutat Res. 1980 Jul;78(3):261-6. doi: 10.1016/0165-1218(80)90107-x.
6
Effect of sodium selenite and methyl methanesulfonate or N-hydroxy-2-acetylaminofluorene co-exposure on sister-chromatid exchange production in human whole blood cultures.亚硒酸钠与甲磺酸甲酯或N-羟基-2-乙酰氨基芴共同暴露对人全血培养物中姐妹染色单体交换产生的影响。
Mutat Res. 1978 Jul;57(3):359-68. doi: 10.1016/0027-5107(78)90220-8.
7
Sister-chromatid exchange induction by sodium selenite: dependence on the presence of red blood cells or red blood cell lysate.亚硒酸钠诱导的姐妹染色单体交换:依赖于红细胞或红细胞裂解物的存在。
Mutat Res. 1978 Dec;54(3):343-54. doi: 10.1016/0165-1161(78)90024-9.
8
Differences in the effects of selenite and biological selenium on the chemical form and distribution of mercury after the simultaneous administration of HgCl2 and selenium to rats.大鼠同时给予氯化汞和硒后,亚硒酸盐和生物硒对汞的化学形态及分布影响的差异。
J Pharmacol Exp Ther. 1984 Feb;228(2):478-83.
9
Induction of sister chromatid exchange by various selenium compounds in Chinese hamster cells in the presence and absence of S9 mixture.在有和没有S9混合物的情况下,各种硒化合物对中国仓鼠细胞姐妹染色单体交换的诱导作用。
Cancer Lett. 1983 Feb;18(1):109-16. doi: 10.1016/0304-3835(83)90124-6.
10
Bis(methylmercuric) selenide as a reaction product from methylmercury and selenite in rabbit blood.
Res Commun Chem Pathol Pharmacol. 1980 Jan;27(1):163-73.

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Toxics. 2021 Dec 1;9(12):326. doi: 10.3390/toxics9120326.
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Use of genetic toxicology data in U.S. EPA risk assessment: the mercury study report as an example.美国环境保护局风险评估中遗传毒理学数据的使用:以汞研究报告为例。
Environ Health Perspect. 1996 May;104 Suppl 3(Suppl 3):663-73. doi: 10.1289/ehp.96104s3663.