铝,一种无处不在的环境毒物,以引发广泛的生理疾病而著称,生物化学,以及实验动物和人类的行为改变。本研究旨在研究铝在大鼠肝脏中引起的功能和结构变化。将25只成年雄性Wistar大鼠(150-200g)随机分为五组;对照组和四个Al处理组,即Al1(25mgAlCl3/kgb.wt),Al2(35mgAlCl3/kgb.wt),Al3(45mgAlCl3/kgb.wt),和Al4(55mgAlCl3/kgb.wt)。铝处理组的大鼠通过口服管饲法给予AlCl330天。铝显着增加肝功能标志物的血清水平(ALT,AST,和ALP),磷脂,和胆固醇。肝细胞膜的活性(ALP,GGT,和LAP)和碳水化合物代谢(G6P,F16BP,香港,LDH,MDH,我,和G6PDH)酶被AlCl3施用显着改变。长时间铝暴露诱导肝脏氧化应激,明显的肝细胞DNA损伤,增加脂质过氧化,和减少非酶和酶抗氧化剂。在这项研究中观察到的毒性作用是AlCl3剂量依赖性的。肝切片的组织病理学检查显示正弦间隙增大,肝弦紊乱,离散肝细胞边界丢失,肝窦充血,和铝中毒大鼠肝细胞的变性。总之,铝通过抑制肝细胞膜酶和破坏肝脏的能量代谢和抗氧化防御引起严重的肝毒性。
Aluminium, a ubiquitous environmental toxicant, is distinguished for eliciting a broad range of physiological, biochemical, and behavioural alterations in laboratory animals and humans. The present work was conducted to study the functional and structural changes induced by aluminium in rat liver. Twenty five adult male Wistar rats (150-200 g) were randomly divided into five groups; control group and four Al-treated groups viz: Al 1 (25 mg AlCl3/kg b.wt), Al 2 (35 mg AlCl3/kg b.wt), Al 3 (45 mg AlCl3/kg b.wt), and Al 4 (55 mg AlCl3/kg b.wt). Rats in the aluminium-treated groups were administered AlCl3 for 30 days through oral gavage. Aluminium significantly increased the serum levels of liver function markers (ALT, AST, and ALP), phospholipids, and cholesterol. The activities of hepatocyte membrane (ALP, GGT, and LAP) and carbohydrate metabolic (G6P, F16BP, HK, LDH, MDH, ME, and G6PDH) enzymes were significantly altered by AlCl3 administration. Prolonged Al exposure induced oxidative stress in the liver, as evident by significant hepatocellular DNA damage, increased lipid peroxidation, and decreased non-enzymatic and enzymatic antioxidants. The toxic effects observed in this study were AlCl3 dose-dependent. Histopathological examination of liver sections revealed enlargement of sinusoidal spaces, derangement of the hepatic chord, loss of discrete hepatic cell boundaries, congestion of hepatic sinusoids, and degeneration of hepatocytes in Al-intoxicated rats. In conclusion, aluminium causes severe hepatotoxicity by inhibiting the hepatocyte membrane enzymes and disrupting the liver\'s energy metabolism and antioxidant defence.