Laboratory of Nutrition - Functional Foods and Vascular Diseases, Faculty of Medicine, University of Monastir, Monastir, 5019, Tunisia.
Laboratory of Histology and Cytogenetic, Faculty of Medicine, University of Monastir, Monastir, 5019, Tunisia.
Environ Sci Pollut Res Int. 2014 Feb;21(3):1648-1657. doi: 10.1007/s11356-013-2057-3. Epub 2013 Aug 16.
The present study aimed to evaluate the effect of arsenic on liver fatty acids (FA) composition, hepatotoxicity and oxidative status markers in rats. Male rats were randomly devised to six groups (n=10 per group) and exposed to sodium arsenate at a dose of 1 and 10 mg/l for 45 and 90 days. Arsenate exposure is associated with significant changes in the FA composition in liver. A significant increase of saturated fatty acids (SFA) in all treated groups (p<0.01) and trans unsaturated fatty acids (trans UFA) in rats exposed both for short term for 10 mg/l (p<0.05) and long term for 1 and 10 mg/l (p<0.001) was observed. However, the cis UFA were significantly decreased in these groups (p<0.05). A markedly increase of indicator in cell membrane viscosity expressed as SFA/UFA was reported in the treated groups (p<0.001). A significant increase in the level of malondialdehyde by 38.3 % after 90 days of exposure at 10 mg/l was observed. Compared to control rats, significant liver damage was observed at 10 mg/l of arsenate by increasing plasma marker enzymes after 90 days. It is through the histological investigations in hepatic tissues of exposed rats that these damage effects of arsenate were confirmed. The antioxidant perturbations were observed to be more important at groups treated by the high dose (p<0.05). An increase in the level of protein carbonyls was observed in all treated groups (p<0.05). The present study provides evidence for a direct effect of arsenite on FA composition disturbance causing an increase of SFA and TFAs isomers, liver dysfunction and oxidative stress. Therefore, arsenate can lead to hepatic damage and propensity towards liver cancer.
本研究旨在评估砷对大鼠肝脏脂肪酸(FA)组成、肝毒性和氧化状态标志物的影响。雄性大鼠被随机分为六组(每组 10 只),分别暴露于 1 和 10mg/L 的砷酸钠 45 和 90 天。砷酸盐暴露与肝脏 FA 组成的显著变化有关。所有处理组的饱和脂肪酸(SFA)显著增加(p<0.01),短期暴露于 10mg/L(p<0.05)和长期暴露于 1 和 10mg/L(p<0.001)的大鼠中转不饱和脂肪酸(trans UFA)也显著增加。然而,这些组中的顺式 UFA 显著减少(p<0.05)。报道称,处理组中细胞膜粘度指标 SFA/UFA 显著增加(p<0.001)。暴露于 10mg/L 90 天后,丙二醛水平显著增加 38.3%。与对照组大鼠相比,暴露于 10mg/L 砷酸盐 90 天后,血浆标记酶水平显著升高,表明肝脏损伤。通过对暴露大鼠肝组织的组织学研究证实了砷酸盐的这些损伤作用。在高剂量处理组中观察到抗氧化剂的波动更为显著(p<0.05)。所有处理组的蛋白羰基水平均升高(p<0.05)。本研究为亚砷酸盐对 FA 组成的直接影响提供了证据,导致 SFA 和 TFAs 异构体增加、肝功能障碍和氧化应激。因此,砷酸盐可导致肝损伤和肝癌倾向。