Al-Quraishy Saleh, Dkhil Mahamed A, Abdel Moneim Ahmed Esmat
Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia ; Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt.
J Venom Anim Toxins Incl Trop Dis. 2014 Sep 15;20(1):42. doi: 10.1186/1678-9199-20-42. eCollection 2014.
Snake venoms are synthesized and stored in venom glands. Most venoms are complex mixtures of several proteins, peptides, enzymes, toxins and non-protein components. In the present study, we investigated the oxidative stress and apoptosis in rat liver cells provoked by Naja haje crude injection (LD50) after four hours.
Wistar rats were randomly divided into two groups, the control group was intraperitoneally injected with saline solution while LD50-dose envenomed group was intraperitoneally injected with venom at a dose of 0.025 μg/kg of body weight. Animals were killed four hours after the injection. Lipid peroxidation, nitric oxide and glutathione levels were measured as oxidative markers in serum and liver homogenate. In addition, liver function parameters and activities of antioxidant enzymes were determined.
N. haje crude venom (0.025 μg/kg of body weight) enhanced lipid peroxidation and nitric oxide production in both serum and liver with concomitant reduction in glutathione, catalase, glutathione reductase and glutathione-S-transferase activities. Superoxide dismutase and glutathione peroxidase activities were significantly increased in liver of envenomed rats. These findings were associated with apoptosis induction in the liver. In addition, N. haje crude venom caused hepatic injury as indicated by histopathological changes in the liver tissue with an elevation in total bilirubin, serum alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transpeptidase, and alkaline phosphatase.
Based on the present results, it can hypothesized that N. haje crude venom is a potent inducer of toxin-mediated hepatotoxicity associated with apoptosis in the liver.
蛇毒在毒腺中合成并储存。大多数毒液是几种蛋白质、肽、酶、毒素和非蛋白质成分的复杂混合物。在本研究中，我们调查了注射埃及眼镜蛇粗毒（半数致死量）4小时后大鼠肝细胞中的氧化应激和细胞凋亡情况。
将Wistar大鼠随机分为两组，对照组腹腔注射生理盐水，而半数致死量剂量中毒组腹腔注射剂量为0.025μg/kg体重的毒液。注射4小时后处死动物。测量血清和肝匀浆中的脂质过氧化、一氧化氮和谷胱甘肽水平作为氧化标志物。此外，还测定了肝功能参数和抗氧化酶活性。
埃及眼镜蛇粗毒（0.025μg/kg体重）增强了血清和肝脏中的脂质过氧化和一氧化氮生成，同时谷胱甘肽、过氧化氢酶、谷胱甘肽还原酶和谷胱甘肽-S-转移酶活性降低。中毒大鼠肝脏中的超氧化物歧化酶和谷胱甘肽过氧化物酶活性显著增加。这些发现与肝脏中的细胞凋亡诱导有关。此外，埃及眼镜蛇粗毒导致肝脏损伤，表现为肝组织的组织病理学变化，总胆红素、血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶和碱性磷酸酶升高。
根据目前的结果，可以推测埃及眼镜蛇粗毒是毒素介导的肝毒性的有效诱导剂，与肝脏中的细胞凋亡有关。
