In vivo formation of chromium(V) in chick embryo liver and red blood cells.
In vivo formation of chromium(V) in chick embryo liver and red blood cells.
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鸡胚肝脏和红细胞中铬（V）的体内形成。
DOI：
10.1093/carcin/13.11.2113
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发表时间：
1992
期刊：
影响因子：
4.7
通讯作者：
Wetterhahn,KE
中科院分区：
文献类型：
--
作者：
Liebross,RH;Wetterhahn,KE
为了了解反应中间体在铬（VI）形成组织特异性DNA损伤中的可能作用，本文用电子顺磁共振（ESR）技术研究了铬（VI）处理14日龄鸡胚后，铬（V）在肝脏和红细胞中的体内形成。在14日龄鸡胚的内壳膜上注入重铬酸钠，可在肝细胞中形成持久的铬（V）物种（g = 1.987）。在用铬（VI）处理后，肝细胞中铬（V）信号的强度在70 mm处达到平台并持续240分钟。铬（V）的形成对剂量的重铬酸钠管理到胚胎的依赖性是明显不同的肝脏与红细胞。仅在高剂量重铬酸钠（0.50-0.60 mmol/kg）下在红细胞中检测到铬（V），而在低剂量重铬酸钠（0.10-0.30 mmol/kg）下在红细胞中检测不到铬（V），这为肝脏中的铬（V）提供了明确的证据。摄取研究表明，红细胞中的总铬水平是肝细胞中的10倍，并且高达10%的总铬以铬（V）的形式存在于体内的肝和红细胞中。在用高剂量重铬酸钠（0.60 mmol/kg）处理前，用L-丁硫氨酸-S，R-亚砜亚胺（BSO）预处理胚胎24 h，使谷胱甘肽耗尽，导致处理后50 min产生的铬（V）物质水平降低，红细胞对铬的摄取减少。在这种高剂量的铬（VI）下，BSO预处理对铬（V）的水平或在70分钟孵育期后对肝细胞的铬摄取没有影响。因此，细胞内铬（V）的浓度与细胞吸收的铬水平相关。铬（V）可能是铬的形式，其负责在体内给予重铬酸钠后诱导DNA损伤。
In order to understand the possible role of reactive intermediates in the formation of tissue-specific DNA damage by chromium(VI), electron paramagnetic resonance spec-troscopy was used to study thein vivoformation of chromium(V) in the liver and red blood cells of 14 day chick embryos following treatment with chromium (VI).In vivoadministration of sodium dichromate onto the inner shell membrane of 14 day chick embryos resulted in the formation of a persistent chromium(V) species in liver cells (g = 1.987). The intensity of the chromium(V) signal in liver cells plateaued at 70 mm and persisted for 240 min after treatment with chromium (VI). The dependence of chromium(V) formation on the dose of sodium dichromate administered to the embryo was clearly different in liver versus red blood cells. Chromium(V) was detected in red blood cells only at high doses of sodium dichromate (0.50–0.60 mmol/kg), whereas chromium(V) was undetectable in red blood cells at lower doses of sodium dichromate (0.10–0.30 mmol/kg) which produced clear evidence for chromium(V) in liver. Uptake studies showed that total chromium levels in red blood cells were 10-fold greater than in liver cells, and that up to 10% of the total chromium existed as chromium(V) in liver and red blood cellsin vivo. Depletion of glutathione by pre-treatment of embryos with L-buthionine-S,R-sulfoximine (BSO) for 24 h prior to treatment with a high dose of sodium dichromate (0.60 mmol/kg) caused both a decrease in the levels of chromium(V) species produced and a decrease of chromium uptake into red blood cells 50 min after treatment. At this high dose of chromium(VI), BSO pre-treatment had no effect on the level of the chromium(V) or on chromium uptake into liver cells after a 70 min incubation period. Thus, the concentration of chromium(V) inside the cell correlated with the levels of chromium taken up into the cell. Chromium(V) may be the form of chromium which is responsible for induction of DNA damage followingin vivoadministration of sodium dichromate.