Sahoo A, Chainy G B
Department of Zoology, S.V.M. College, Orissa, India.
Neurochem Res. 1998 Aug;23(8):1079-84. doi: 10.1023/a:1020760119541.
Hexachlorocyclohexane (HCH) is reported to induce oxidative stress in liver and testis of rat. With an objective to examine its effect on brain tissue acute toxicity of HCH (10 and 20 mg/kg body wt, i.p.) on the antioxidant defense system of cerebral hemisphere of rat was evaluated. Lipid peroxidation (LPX) was elevated after 24 h in the crude homogenate and sub-cellular fractions (nuclear and mitochondrial) except the microsomal fraction in which LPX was induced after 6 h and remained elevated till 24 h. The pesticide elicited decrease in the activities of cytosolic total, CN(-)-sensitive (not at 24 h) and CN-resistant superoxide dismutases; total, Se-dependent and Se-independent glutathione peroxidases; and catalase throughout the measurement period. In contrast, glutathione reductase activity was elevated till 24 h after a fall at 6 h of pesticide exposure. Cerebral contents of glutathione and ascorbic acid were decreased in response to HCH. The results suggest the possible involvement of reactive oxygen species in the mechanism of HCH-induced neurotoxicity in rat.
据报道,六氯环己烷(HCH)可诱导大鼠肝脏和睾丸中的氧化应激。为了研究其对脑组织的影响,评估了HCH(10和20毫克/千克体重,腹腔注射)对大鼠大脑半球抗氧化防御系统的急性毒性。24小时后,粗匀浆和亚细胞组分(细胞核和线粒体)中的脂质过氧化(LPX)升高,但微粒体组分除外,其中LPX在6小时后诱导并持续升高至24小时。在整个测量期间,该农药导致胞质总超氧化物歧化酶、对氰化物敏感(24小时时未出现)和对氰化物抗性的超氧化物歧化酶活性降低;总谷胱甘肽过氧化物酶、硒依赖性和非硒依赖性谷胱甘肽过氧化物酶活性降低;过氧化氢酶活性降低。相反,谷胱甘肽还原酶活性在农药暴露6小时下降后升高至24小时。谷胱甘肽和抗坏血酸的脑含量因HCH而降低。结果表明活性氧可能参与了HCH诱导大鼠神经毒性的机制。