Rana Tanmoy, Bera Asit Kumar, Bhattacharya Debasis, Das Subhashree, Pan Diganta, Das Subrata Kumar
Indian Veterinary Research Institute, Eastern Regional Station, Kolkata-37, West Bengal, India.
Indian Veterinary Research Institute, Eastern Regional Station, Kolkata-37, West Bengal, India National Research Centre on Yak, Dirang, West Kameng District, Arunachal Pradesh- 790101, India
Toxicol Ind Health. 2015 Feb;31(2):108-22. doi: 10.1177/0748233712468026. Epub 2013 Jan 2.
Arsenic is one of the most hazardous substances in the environment known to cause toxicity in multiple organs. Cell adhesion, morphological alterations, cell proliferation, terminal deoxyuridine triphosphate nick-end labeling (TUNEL) and caspase-3/CPP32 fluorometric protease assay were important biomarkers to assess apoptosis in cells. This study aimed to evaluate arsenic-induced apoptosis in the hepatocytes of rat and its protective efficacy with coadministration of ascorbic acid (AA) and Pleurotus florida lectin (PFL) individually. Results of the present study also showed that arsenic caused cytotoxicity by elevating morphological alterations, TUNEL-positive nuclei, caspase-3 activity and DNA damage and reducing cell adhesion and cell proliferation in a time-dependent manner. The apoptosis in hepatocytes was reverted to normal value after coadministration of mushroom lectin in arsenic-exposed rat. The study provided significant evidence that PFL has antiapoptotic property against arsenic-induced toxicity. The beneficial effect of PFL was proportional to its duration of exposure. Retard activities of superoxide dismutase and catalase, enhanced lipid peroxidation as well as protein carbonyl in erythrocytes caused by arsenic could also be maintained toward normalcy by supplementation of AA and PFL. These antioxidative effects were exhibited in a time-dependant manner. In rat, treatment with AA and PFL prevented alteration of plasma enzyme activities caused by arsenic. The results concluded that treatment with PFL has significant role in protecting animals from arsenic-induced erythrocytic damage. This finding might be of therapeutic benefit in people suffering from chronic exposure to arsenic from natural sources, a global problem especially relevant to millions of people on the Indian subcontinent.
砷是环境中最危险的物质之一，已知会对多个器官造成毒性。细胞黏附、形态改变、细胞增殖、末端脱氧尿苷三磷酸缺口末端标记法（TUNEL）和半胱天冬酶-3/CPP32荧光蛋白酶检测是评估细胞凋亡的重要生物标志物。本研究旨在分别评估砷诱导大鼠肝细胞凋亡的情况以及抗坏血酸（AA）和佛罗里达侧耳凝集素（PFL）共同给药的保护效果。本研究结果还表明，砷通过增加形态改变、TUNEL阳性细胞核、半胱天冬酶-3活性和DNA损伤，并以时间依赖性方式降低细胞黏附和细胞增殖，从而导致细胞毒性。在砷暴露的大鼠中共同给予蘑菇凝集素后，肝细胞凋亡恢复到正常水平。该研究提供了重要证据，表明PFL对砷诱导的毒性具有抗凋亡特性。PFL的有益作用与其暴露持续时间成正比。补充AA和PFL也可使砷引起的红细胞中超氧化物歧化酶和过氧化氢酶活性降低、脂质过氧化增强以及蛋白质羰基化恢复正常。这些抗氧化作用呈时间依赖性表现。在大鼠中，用AA和PFL治疗可防止砷引起的血浆酶活性改变。结果得出结论，用PFL治疗在保护动物免受砷诱导的红细胞损伤方面具有重要作用。这一发现可能对长期接触天然来源砷的人群具有治疗益处，这是一个全球性问题，尤其与印度次大陆数百万人口相关。
