Mechanism of cellular damages caused by cholorophenol compounds and their prevention

五氯苯酚（PCP）增加了大鼠肝脏线粒体的耗氧量，降低了呼吸控制率（J .中华医学会杂志，1998）。左旋肉碱能抑制PCP的这些作用，而戊四唑（PTZ）则没有。我们的其他发现包括；n -乙酰半胱氨酸对细胞毒性的影响[J]； contemporary medicine; 2009；镉在相同细胞中激活c-Jun n -末端激酶（JNX）（生物化学，生物物理学报，251:527,1998）；肉碱抑制ptz诱导的小鼠脑内c-fos表达（J Occup Health, in press）；镉的毒性在缺乏c-fos的成纤维细胞中更大（Biochem Pharmacol, in press）。然而，缺乏c-fos的细胞对PCP和六氯酚（HCP）的反应与对照组没有明显差异。PCP和HCP均未引起JNK、ERK和p-38的明显激活，提示c-Fos和c-Jun的信号转导系统可能未参与上述氯酚类化合物的毒性诱导。然而，左旋肉碱可能会减轻PCP对线粒体的毒性。

Pentachloropheno1 (PCP) increased oxygen consumption and decreased repiratory control ratio in mitochondria from rat liver (J UOEH 20:315, 1998). These effects of PCP were suppressed by L-carnitine but those of pentylenetetrazol (PTZ) were not. Other findings of ours include ; N-acetylcysteine suppressed cytotoxicity of cadmium in LLC-PK1 cells (J Pharmacol Exp Therap 287:344, 1998) ; cadmium activated c-Jun N-terminal kinase (JNX) in the same cells (Biochem Biphys Res Commun 251:527, 1998) ; carnitine suppressed PTZ-induced c-fos expression in the mouse brain (J Occup Health, in press) ; toxicity of cadmium was greater in fibroblasts lacking c-fos (Biochem Pharmacol, in press). Nevertheless, cells lacking c-fos showed no definite difference from the controls in response to PCP and hexachlorophene (HCP). Neither PCP nor HCP caused clear activation of JNK, ERK and p-38, suggesting that signal transduction system to c-Fos and c-Jun may not be involved in inducing cellar toxicity of above chlorophenol compounds. However, it is likely that toxicity of PCP on mitochondria may be lessened by L-carnitine.