Protective Effects of N-Acetylcysteine on Hepatic and Renal Oxidative Injury in a Propylthiouracil-Induced Hypothyroid Rat Model

Introduction: Hypothyroidism is a prevalent endocrine disorder characterized by insufficient thyroid hormone production and a substantial decline in quality of life. It is closely associated with increased oxidative stress, which may induce functional and structural damage in multiple organs, including the liver and kidneys. This study investigated the effects of N-Acetylcysteine (NAC), a potent antioxidant, on hepatic and renal tissue damage in a Propylthiouracil (PTU)-induced hypothyroid rat model. Method: A total of ۴۸ male Wistar rats offspring were randomly allocated to six groups, including a control group, a PTU-induced hypothyroid group, three hypothyroid groups treated with NAC (۵۰, ۱۰۰, and ۱۵۰ mg/kg/day), and an NAC-only control group. oxidative stress parameters in liver and renal tissues were measured. Also, liver, renal and Thyroid Function Tests were done. Results: Biochemical assessments revealed that NAC administration dose-dependently increased serum thyroxine (T۴) levels and significantly reduced serum creatinine, blood urea nitrogen, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels compared with untreated hypothyroid rats (P < ۰.۰۵–۰.۰۰۱). Additionally, NAC result in reduction in oxidative stress markers, including malondialdehyde (MDA) and nitrite levels, while significantly enhancing the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) in both hepatic and renal tissues. Overall, these findings suggest that NAC effectively attenuates oxidative stress–mediated hepatic and renal injury in hypothyroidism, highlighting its potential therapeutic role as an adjunct treatment.

کلیدواژه ها:

N-Acetylcysteine ، Oxidative stress ، Hypothyroidism ، Hepatic injury ، Renal dysfunction