Neurophysiology Laboratory Division of Physiology & Climatology, Indian Veterinary Research Institute, Izatnagar, 243122 Uttar Pradesh, India.
Biol Trace Elem Res. 2012 May;146(2):224-9. doi: 10.1007/s12011-011-9245-0. Epub 2011 Nov 18.
Arsenic (As) toxicity through induction of oxidative stress is a well-known mechanism of organ toxicity. To address this problem, buffalo epiphyseal proteins (BEP, at 100 μg/kg BW, i.p. for 28 days) were administered intraperitoneally to female Wistar rats exposed to As (100 ppm sodium arsenite via drinking water for 28 days). Arsenic exposure resulted in marked elevation in lipid peroxidation in brain, cardiac, and hepatic tissues, whereas significant (p < 0.05) adverse change in catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase, and reduced glutathione level were observed in cardiac, hepatic, and brain tissues of As-administered animals. BEP significantly (p < 0.05) counteracted all the adverse changes in antioxidant defense system brought about by As administration. Based on these results, we consider BEP as a potent antioxidant to be used for protection from arsenic-induced oxidative stress related damage of vital organs.
砷（As）通过诱导氧化应激引起的毒性是器官毒性的已知机制。为了解决这个问题，向接触砷的雌性 Wistar 大鼠（通过饮用水摄入 100ppm 亚砷酸钠，持续 28 天）腹腔内注射水牛骨骺蛋白（BEP，剂量为 100μg/kgBW，持续 28 天）。砷暴露导致大脑、心脏和肝脏组织中的脂质过氧化明显升高，而在给予砷的动物的心脏、肝脏和大脑组织中，过氧化氢酶、超氧化物歧化酶、谷胱甘肽还原酶、谷胱甘肽过氧化物酶和还原型谷胱甘肽水平发生了显著（p<0.05）的不利变化。BEP 显著（p<0.05）抵消了砷给药引起的抗氧化防御系统的所有不利变化。基于这些结果，我们认为 BEP 是一种有效的抗氧化剂，可用于防止砷引起的氧化应激对重要器官的损伤。
