Investigation of the effect of acrylamide administration on aromatase gene expression in muscle and adipose tissues of adult male rats

Aim: AKR is a chemical with toxic effects that is not naturally found in foods but is frequently encountered in daily life as a result of high-temperature cooking. Aromatase, encoded by the CYP19A1 gene, catalyzes the conversion of androgens into estrogens. Our objective is to investigate the effects of AKR exposure on aromatase gene expression in the muscle and adipose tissues of adult male rats. Additionally, this research aims to explore the potential protective effects of vitamin E against the male reproductive health-damaging impacts caused by AKR. Material and Method: In this study, 48 adult male Sprague Dawley rats, 8 weeks old and weighing 200 ± 30 g, were used. The rats were divided into 5 groups: Group 1: Control group (8 rats), Group 2: Corn oil group (8 rats), Group 3: Vitamin E group (8 rats), Group 4: AKR group (12 rats), and Group 5: AKR + Vitamin E group (12 rats). In the treatment groups, AKR was administered through drinking water, while vitamin E and corn oil were given via oral gavage for 56 days. The control group was fed ad libitum, with unlimited access to food and water. At the end of the 56 days, blood, muscle, and adipose tissue samples were collected and preserved under appropriate conditions. Aromatase gene expression in tissue samples was analyzed using the Western Blot method. Serum samples were analyzed for testosterone, östradiol, FSH, and LH levels using the ELISA method. Additionally, during the study period, live animal weights and the rats' food and water consumption were recorded weekly. Results: The analysis results revealed that acrylamide caused significant increases in muscle and adipose aromatase expression and significantly increased FSH secretion while reducing testosterone levels. Treatment with vitamin E partially restored these parameters toward control levels. Conclusion: All these findings demonstrate the detrimental effects of AKR exposure on the male reproductive system at the molecular level and suggest that AKR may contribute to infertility.