Medical Laboratories Technology Department, Faculty of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia.
Ecotoxicol Environ Saf. 2012 Sep;83:47-54. doi: 10.1016/j.ecoenv.2012.06.003. Epub 2012 Jul 4.
Beryllium chloride (BeCl(2)) is a highly toxic substance that accumulates in different tissues after absorption. The purpose of this study was to investigate protective role of crocin against BeCl(2)-intoxication in rats. Male Wistar rats were used in this study and categorised into four groups (n=8). Group I served as normal control rats. Group II treated orally with BeCl(2) 86 mg/kg b.w. for five consecutive days. This dose was equivalent to experimental LD(50). Group III treated intraperitoneally with crocin 200 mg/kg b.w. for seven consecutive days. Group IV received crocin for seven consecutive days before BeCl(2) administration. Blood samples and liver and brain homogenates were obtained for haematological, biochemical and RT-PCR examinations. The haematocrit value, RBCs count and haemoglobin concentration were significantly decreased in BeCl(2)-treated rats. A significant increase was observed in rat liver and brain malondialdehyde level and protein carbonyls content in BeCl(2) exposed group compared to the control group, and these values were significantly declined upon administration of crocin. Lactate dehydrogenase levels in rat liver and brain significantly increased compared to the control group and was associated with significant decrease in catalase and superoxide dismutase activities. Reduced glutathione hepatic contents of BeCl(2)-treated rats were significantly decreased. There was significant decline in mRNA expression of catalase and superoxide dismutase genes in BeCl(2)-intoxicated rats compared to the normal rats. Crocin treatment prior to BeCl(2) intake resulted in significant increase in mRNA expressions of catalase and superoxide dismutase genes near to normalcy. The haematological and biochemical parameters were restored near to normal levels. Our results suggested that, BeCl(2) induced oxidation of cellular lipids and proteins and that administration of crocin reduced BeCl(2)-induced oxidative stress combined with initiation of mRNA expression of antioxidant genes.
氯化铍（BeCl(2)）是一种高度毒性物质，吸收后会在不同组织中积累。本研究旨在探讨藏红花酸对大鼠氯化铍中毒的保护作用。雄性 Wistar 大鼠用于本研究，并分为四组（n=8）。第 I 组作为正常对照组。第 II 组连续 5 天口服给予 86mg/kg b.w.的氯化铍。此剂量相当于实验性 LD(50)。第 III 组连续 7 天腹腔内给予 200mg/kg b.w.的藏红花酸。第 IV 组在给予氯化铍前连续 7 天给予藏红花酸。采集血液样本和肝脑匀浆进行血液学、生化和 RT-PCR 检查。与对照组相比，氯化铍处理组的红细胞压积值、红细胞计数和血红蛋白浓度明显降低。与对照组相比，氯化铍暴露组大鼠肝脑丙二醛水平和蛋白质羰基含量显著升高，给予藏红花酸后这些值显著下降。与对照组相比，大鼠肝脑乳酸脱氢酶水平显著升高，与过氧化氢酶和超氧化物歧化酶活性显著下降相关。氯化铍处理组大鼠肝还原型谷胱甘肽含量明显降低。与正常大鼠相比，氯化铍中毒大鼠过氧化氢酶和超氧化物歧化酶基因的 mRNA 表达显著降低。在摄入氯化铍之前给予藏红花酸处理可导致过氧化氢酶和超氧化物歧化酶基因的 mRNA 表达显著增加，接近正常水平。血液学和生化参数恢复到接近正常水平。我们的结果表明，氯化铍诱导细胞脂质和蛋白质氧化，而给予藏红花酸可减轻氯化铍诱导的氧化应激，同时启动抗氧化基因的 mRNA 表达。
