The role of mitochondrial glutathione and cellular protein sulfhydryls in formaldehyde toxicity in glutathione-depleted rat hepatocytes.
The role of mitochondrial glutathione and cellular protein sulfhydryls in formaldehyde toxicity in glutathione-depleted rat hepatocytes.
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线粒体谷胱甘肽和细胞蛋白巯基在谷胱甘肽耗尽的大鼠肝细胞甲醛毒性中的作用。
DOI：
10.1016/0003-9861(86)90547-3
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发表时间：
1986
影响因子：
3.9
通讯作者：
Billings,RE
中科院分区：
文献类型：
--
作者：
Ku,RH;Billings,RE
马来酸二乙酯（DEM）对细胞GSH的消耗增强了离体大鼠肝细胞中CH2O的毒性，据推测，这种毒性的增加是由于在DEM预处理的肝细胞中CH2O导致GSH的进一步降低(1)。本研究旨在进一步研究CH2O、DEM和丙烯醛（一种结构上与CH2O和DEM相关的化合物）对亚细胞GSH池和蛋白质巯基（PSH）的影响。CH2O引起细胞质GSH的降低，但对先前未治疗的肝细胞或经dm预处理的肝细胞（GSH约为对照组的25%）的线粒体GSH没有影响。DEM降低细胞质和线粒体GSH，但不产生毒性。CH2O （7.5 mm）和DEM （20 mm）均未降低PSH。然而，在用1mmdem预处理的细胞中，CH2O （7.5 mm）降低了PSH，这种作用先于细胞死亡。丙烯醛降低细胞质和线粒体GSH，并在引起细胞死亡前显著降低PSH。CH2O和丙烯醛分别通过psh非依赖性和psh依赖性机制刺激磷酸化酶活性，表明胞质游离Ca2+增加。这些结果表明，在dem预处理的细胞中，CH2O对细胞GSH的进一步消耗不是由于线粒体GSH的消耗。然而，在dem预处理的细胞中CH2O毒性与PSH的消耗相关。导致细胞死亡的关键巯基蛋白仍有待更明确的定义。
Depletion of cellular GSH by diethyl maleate (DEM) potentiates CH2O toxicity in isolated rat hepatocytes and it was postulated that this increase in toxicity is due to the further decrease in GSH caused by CH2O in DEM-pretreated hepatocytes (1). The present investigation was conducted to investigate further the effects of CH2O, DEM, and acrolein (a compound which is structurally related to CH2O and DEM) on subcellular GSH pools and on protein sulfhydryl groups (PSH). CH2O caused a decrease in cytosolic GSH but had no effect on mitocnondrial GSH either in previously untreated hepatocytes or in DEM-pretreated hepatocytes in which GSH was approximately 25% of control. DEM decreased both cytosolic and mitochondrial GSH but it did not produce toxicity. Neither CH2O (up to 7.5 mm) nor DEM (20 mm) decreased PSH. However, in cells pretreated with 1 mmDEM, CH2O (7.5 mm) decreased PSH and this effect preceded cell death. Acrolein decreased both cytosolic and mitochondrial GSH and it also decreased PSH significantly prior to causing cell death. CH2O and acrolein stimulated phosphorylaseaactivity, indicative of an increase in cytosolic free Ca2+, by a PSH-independent and PSH-dependent mechanism, respectively. These results suggest that the further depletion of cellular GSH by CH2O in DEM-pretreated cells is not due to the depletion of mitochondrial GSH. CH2O toxicity in DEM-pretreated cells is, however, correlated with depletion of PSH. The critical sulfhydryl protein(s) responsible for cell death remain to be more clearly defined.
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影响因子：
5.1
作者：
KU, RH;BILLINGS, RE
通讯作者：
BILLINGS, RE
离体肝细胞中甲醇毒性和甲酸代谢的研究。
影响因子：
5.8
作者：
R. Billings;T. Tephly
通讯作者：
T. Tephly
DOI：
10.1016/0006-291x(76)90335-1
发表时间：
1976-01-01
影响因子：
3.1
作者：
HIGASHI, T;TATEISHI, N;SAKAMOTO, Y
通讯作者：
SAKAMOTO, Y
烯丙醇和丙烯醛在大鼠肝和肺制剂中的生物转化。
影响因子：
3.9
作者：
J. M. Patel;J. C. Wood;K. Leibman
通讯作者：
K. Leibman
DOI：
10.1016/s0074-7696(08)60166-7
发表时间：
1978-01-01
期刊：
International review of cytology
影响因子：
--
作者：
Kosower, N S;Kosower, E M
通讯作者：
Kosower, E M