Benzoyl peroxide cytotoxicity evaluated in vitro with the human keratinocyte cell line, RHEK-I
Benzoyl peroxide cytotoxicity evaluated in vitro with the human keratinocyte cell line, RHEK-I
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DOI：
10.1016/0300-483x(95)03189-m
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发表时间：
1996-01-08
期刊：
影响因子：
4.5
通讯作者：
Blau, L
中科院分区：
文献类型：
--
作者：
Babich, H;Zuckerbraun, HL;Blau, L
使用人角质形成细胞系RHEK-1评价过氧化苯甲酰（BZP）的细胞毒性。如中性红（NR）细胞毒性试验所测定，BZP的24小时中点（NR（50））毒性值（mM）为0.11，苯甲酸（BZP的稳定代谢产物）为29.5。暴露于0.15 mM BZP或更高浓度1小时后发生不可逆的细胞毒性。当暴露于BZP 7天时，在0.06 mM BZP下首先观察到生长动力学滞后。质膜完整性的损伤是明显的，因为在暴露于0.05 mM BZP或更高浓度4小时期间发生乳酸脱氢酶泄漏。细胞内膜也受到影响，因为在BZP应激细胞中注意到广泛的空泡化，最初是核周的，但随后扩散到整个细胞质。BZP引起的活性自由基的产生主要表现在：BZP使细胞内谷胱甘肽含量降低，经谷胱甘肽耗竭剂氯二硝基苯预处理的细胞对BZP的刺激反应敏感，Fe ~（2+）可诱导BZP引起的脂质过氧化反应，Fe ~（2+）可诱导BZP引起的脂质过氧化反应。而先前在添加了维生素E（一种抗氧化剂）的培养基中培养的细胞，对BZP的抗性更强，在BZP + Fe 2+存在下，显示较少的脂质过氧化作用，并且与非BZP + Fe 2+相比，没有发生广泛的细胞内空泡化。维生素E维持细胞。
The human keratinocyte cell line, RHEK-1, was used to evaluate the cytotoxicity of benzoyl peroxide (BZP). As determined with the neutral red (NR) cytotoxicity assay, the 24-h midpoint (NR(50)) toxicity values, in mM, were 0.11 for BZP and 29.5 for benzoic acid, the stable metabolite of BZP. Irreversible cytotoxicity occurred after a I-h exposure to 0.15 mM BZP and greater, When exposed to BZP for 7 days, a lag in growth kinetics was first observed at 0.06 mM BZP, Damage to the integrity of the plasma membrane was evident, as leakage of lactic acid dehydrogenase occurred during a 4-h exposure to BZP at 0.05 mM and greater. Intracellular membranes were also affected, as extensive vacuolization, initially perinuclear but then spreading throughout the cytoplasm, was noted in BZP-stressed cells. The generation of reactive free radicals from BZP was suggested by the following: the intracellular content of glutathione was lowered in cells exposed to BZP; cells pretreated with the glutathione-depleting agent, chlorodinitrobenzene, were hypersensitive to a subsequent challenge with BZP; lipid peroxidation by BZP was inducible in the presence of Fe2+; and cells previously maintained in a medium amended with vitamin E, an antioxidant, were more resistant to BZP, showed less lipid peroxidation in the presence of BZP + Fe2+ and did not develop the extensive intracellular vacuolization as compared to non-vitamin E maintained cells.