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左旋肉碱对大鼠实验性铅中毒的保护作用:一项临床、组织病理学和免疫组织化学研究。

Protective effect of L-carnitine on experimental lead toxicity in rats: a clinical, histopathological and immunohistochemical study.

作者信息

Ozsoy S Y, Ozsoy B, Ozyildiz Z, Aytekin I

机构信息

Faculty of Veterinary Medicine, Department of Pathology, Mustafa Kemal University, Hatay, Turkey.

出版信息

Biotech Histochem. 2011 Dec;86(6):436-43. doi: 10.3109/10520295.2010.529825. Epub 2010 Nov 2.

DOI:10.3109/10520295.2010.529825
PMID:21039307
Abstract

Female Wistar-albino rats were given lead acetate (PbAc) for 60 days to investigate the protective effects of L-carnitine (CA) clinically and histopathologically on PbAc-induced tissue damage. Blood samples were obtained from the jugular vein for hemoglobin (HB), hematocrit (HCT), red blood cells (RBC), white blood cells (WBC), platelets (PLT), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine. PbAc treatment caused a significant decrease in HB, HCT and RBC, a significant increase in WBC, AST, ALT and creatinine compared to controls. Although administration of CA did not reverse HB and HCT values, it reversed both the decrease in RBC and the increase in WBC, AST, ALT and creatinine. After the experimental period, all rats were weighed, then decapitated for pathological examination. Control rat liver, kidney and brain showed normal histological architecture. Lead-induced nephropathic kidneys; degenerative changes, inflammation and portal edema of the liver; and brain neuropil vacuolation, neuronal vacuolation, satellitosis and neuronophagia were observed in experimental groups. All changes were reduced in the PbAc group treated with CA (PbAc + CA). PbAc caused copper/zinc superoxide dismutase (Cu/Zn-SOD) expression in both the hepatocytes and tubular epithelium of the kidney. PbAc + CA exposure caused moderate Cu/Zn-SOD immunoreactivity. While in the brain sections of the PbAc group the degenerative neurons were stained intensely with anti-ubiquitin antibody, PbAc + CA rats showed moderate staining in neurons with anti-ubiquitin antibody. These results show that CA as a food additive reduced the severity of tissue damage caused by PbAc.

摘要

给雌性Wistar白化大鼠喂食醋酸铅(PbAc)60天,以临床和组织病理学方式研究左旋肉碱(CA)对PbAc诱导的组织损伤的保护作用。从颈静脉采集血样,检测血红蛋白(HB)、血细胞比容(HCT)、红细胞(RBC)、白细胞(WBC)、血小板(PLT)、天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)和肌酐。与对照组相比,PbAc处理导致HB、HCT和RBC显著降低,WBC、AST、ALT和肌酐显著升高。虽然给予CA并未使HB和HCT值恢复正常,但它使RBC的降低以及WBC、AST、ALT和肌酐的升高均得到了逆转。实验期结束后,称量所有大鼠体重,然后断头进行病理检查。对照大鼠的肝脏、肾脏和大脑显示出正常的组织学结构。实验组观察到铅诱导的肾病性肾脏;肝脏的退行性变化、炎症和门静脉水肿;以及大脑神经纤维网空泡化、神经元空泡化、卫星现象和噬神经元现象。在用CA处理的PbAc组(PbAc + CA)中,所有变化均减轻。PbAc导致肝细胞和肾小管上皮细胞中铜/锌超氧化物歧化酶(Cu/Zn-SOD)表达。PbAc + CA暴露导致中度的Cu/Zn-SOD免疫反应性。在PbAc组的脑切片中,退行性神经元用抗泛素抗体染色强烈,而PbAc + CA组大鼠的神经元用抗泛素抗体染色为中度。这些结果表明,CA作为一种食品添加剂减轻了PbAc所致组织损伤的严重程度。

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