Quercetin reverses testicular damage caused by an increase in nitric oxide in an experimental model of Metabolic Syndrome.

Abstract

Metabolic Syndrome (MS) causes damage to the male reproductive system. Previous studies have shown that oxidative stress in the testes, decreased serum testosterone levels, and lower sperm concentration and motility triggered by MS can be prevented by Quercetin (Qc). The aim of this work was to investigate the involvement of nitric oxide (NO) in the testicular damage induced by MS and to assess the potential protective effects of Qc. Adult male Wistar rats were divided into four groups: control (C) group, MS group (given water with 10% fructose for 8 weeks), MS+Qc group (50 mg Qc/kg body weight, orally administered for 2 weeks prior to the end of the experiment), and C+Qc group (50 mg Qc/kg body weight, orally administered for the last 2 weeks). MS markers, anthropometric parameters, and testicular weight index (IPT) were measured. Seminiferous tubules histology and spermatogenesis were evaluated using hematoxylin-PAS staining. NO content in testicular homogenates was determined using the Griess technique. The data were analyzed using ANOVA and the Tukey's post-hoc test, with p<0.05 considered significant. MS was characterized by an increase in body weight, waist circumference, body mass index, and triglycerides, as well as a decrease in HDL-cholesterol. Animals with MS showed complete spermatogenesis, but they presented an increase in IPT and histological changes such as larger seminiferous tubule areas (C:103±5.47; SM:141.2±6.99*; SM+Qc:117.03±1.02 x10³ μm²; *p<0.05 vs C and SM+Qc) and germ cell layer widths with the presence of vacuoles (C: 95.7±4.58; SM: 116.4±4.46 *; SM + Qc:100.24±4.46 μm; * p<0.55 vs C, and SM+Qc). The MS group also had higher NO content compared to the control group, and Qc administration reversed this increase (C:8.44±1.60; MS:17.14±0.91*; MS+Qc:11.3±1.71 μmol nitrite/mg protein; *p<0.05 vs C and MS +Qc). The studied variables in the C+Q group were identical to the C group. All these findings together suggest that NO production is a contributing factor to the testicular deterioration caused by MS, and Qc may offer protection against it