Bianchini Adalto, Monserrat José Maria
Departamento de Ciências Fisiológicas, Fundação Universidade Federal do Rio Grande, Campus Carreiros, Av. Itália km 8, Rio Grande, RS, 96-201-900, Brazil.
Ecotoxicol Environ Saf. 2007 May;67(1):100-8. doi: 10.1016/j.ecoenv.2006.03.006. Epub 2006 May 3.
The protective role of sesamol, an inhibitor of the mixed function oxygenase (MFO) system, against histopathological effects of methyl parathion in the hepatopancreas of the estuarine crab, Chasmagnathus granulatus, was studied. Exposure (72 h) to a sublethal dose (0.05 mg/kg/day; 10% of 72 h-LD50) of injected methyl parathion increased the percentage of damaged hepatopancreatic tubules. Presence of melanin-like deposits in the connective tissue between hepatopancreatic tubules was also observed. Antioxidant enzyme activities (catalase and glutathione S-transferase) and lipid peroxidation (LPO) levels were also increased in hepatopancreas of crabs injected with methyl parathion. Pretreatment with sesamol (0.85 mg/kg/day) significantly protected against all these effects. These findings suggest that the hepatopancreatic damages induced by methyl parathion are due to LPO of hepatopancreatocytes membranes, as a consequence of the oxidative stress generated after methyl parathion oxidative biotransformation mediated by the MFO system.
研究了混合功能氧化酶（MFO）系统抑制剂芝麻酚对河口蟹颗粒厚蟹肝胰腺中甲拌磷组织病理学影响的保护作用。注射亚致死剂量（0.05 mg/kg/天；72小时半数致死剂量的10%）的甲拌磷72小时后，肝胰腺受损小管的百分比增加。在肝胰腺小管之间的结缔组织中也观察到了类黑色素沉积物。注射甲拌磷的蟹肝胰腺中的抗氧化酶活性（过氧化氢酶和谷胱甘肽S-转移酶）和脂质过氧化（LPO）水平也有所增加。用芝麻酚（0.85 mg/kg/天）预处理可显著预防所有这些影响。这些发现表明，甲拌磷诱导的肝胰腺损伤是由于MFO系统介导的甲拌磷氧化生物转化后产生的氧化应激导致肝胰腺细胞膜的脂质过氧化所致。
