Liver Function of Male Rats Exposed to Manganese at Different Time Points
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Liver Function of Male Rats Exposed to Manganese at Different Time Points Xiaonian Zhu 1 & Lin Yang 1 & Yonghua He 1 & Yi Sun 1 & Wenxiang Shi 1 & Chaoyan Ou 1 Received: 17 December 2019 / Accepted: 30 January 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract As an essential trace element in the human body, manganese (Mn) is involved in many important biochemical reactions. However, excessive exposure to manganese can cause multiple systematic damages to the body. This study aims to investigate the effects of manganese exposure on serum hepatic enzymes in male rats at different time points. After adaptive feeding for 7 days, male Sprague–Dawley (SD) rats were injected intraperitoneally with 30 mg/kg MnCl2·4H2O once a day for 21 days at zeitgeber time point 2 (ZT2), ZT8, ZT14, and ZT20, respectively. We found that short-term repeated exposure to manganese caused slower body weight gain and increased relative liver and spleen weight index in male rats at different time points. Moreover, serum total bile acid (TBA) increased while aspartate aminotransferase (AST) decreased at ZT2, ZT8, and ZT20. Cholinesterase (ChE) decreased at ZT2 and ZT20, lactic dehydrogenase (LDH) decreased at ZT2, ZT14, and ZT20, and acid phosphatase (ACP) decreased at ZT2 and ZT14. Alkaline phosphatase (ALP) decreased at ZT2, ZT14, and ZT20, but increased at ZT8. Alanine amino transferase (ALT) decreased at ZT2 and ZT20, but increased at ZT8. There was a negative correlation between relative liver weight index with AST, ACP, ALP, and LDH, while a positive correlation with TBA. However, relative spleen weight index had a positive correlation with relative liver weight index and TBA, while a negative correlation with ALT, AST, ACP, ALP, LDH, and ChE. Our study shows that the injury of liver function is caused by short-term repeated manganese exposure at different time points. The time effect should be considered in manganese toxicity evaluation. Keywords Manganese . Time toxicity . Liver function injury . Serum hepatic enzymes . Short-term repeated exposure
Introduction Manganese (Mn) is an essential trace element in the human body. As a structural component, an activating factor, or cofactor of various enzymes in animals, manganese is involved in many important biochemical reactions [1]. However, excessive exposure to manganese can cause multiple systematic damages to the body. Manganese enters the body and deposits in the liver through binding to mitochondria. The liver is the main accumulation and target organ of manganese, only second to the brain [2]. Manganese excessive exposure could cause slight congestion in the hepatic central vein and adjacent sinus tubules, a focal necrotic area composed of denatured hepatocytes and inflammatory cells, disappearance of mitochondrial extracorporeal
* Chaoyan Ou [email protected] 1
Department of Health Toxicology, School of Public Health, Guilin Medical University, 109 Huancheng North Road 2, Guilin, Guangxi 541004, People’s Republic of China
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