ABSTRACT
OBJECTIVE: Atrazine (ATZ) as a widely used herbicide is considered as a potent endocrine disrupter which adversely affects reproductive systems in both genders. This study aimed to assess the effects of testosterone (T)- and vitamin E (VitE)- alone and their coadministration on testicular function and sperm parameters after exposure to ATZ in rats. MATERIALS AND METHODS: In this experimental study, the rats (n=30) are assigned into the following 5 groups: control-sham group (n=6) receiving corn oil, ATZ group (n=6) receiving 200 mg/kg ATZ alone, ATZ+VitE group (n=6) receiving 150 mg/kg ATZ+VitE, ATZ+T group (n=6) receiving 400 µg/kg ATZ+T, and ATZ+VitE+T group (n=6) receiving ATZ+VitE+T for 48 consecutive days. Total antioxidant capacity (TAC), total thiol molecules (TTM), and malondialdehyde (MDA) were analyzed. Serum levels of T, luteinizing hormone (LH), and inhibin-B (IN-B) were also determined. Histological examination and sperm analysis were performed. The data were analyzed using Graph-Pad Prism software version 2.01. RESULTS: Co-administration of VitE and T significantly (P<0.05) increased ATZ-decreased TAC and TTM levels and reduced ATZ-increased MDA content. T and VitE significantly (P<0.05) increased serum levels of ATZ-reduced T (1.94 ± 0.96), IN-B (122.10 ± 24.33) and LH (0.40 ± 0.10). The T+VitE animals showed a reduction in apoptotic cells and an increase in Leydig cells steroidogenesis. Co-administration of T and VitE significantly (P<0.05) reduced the ATZ-induced DNA disintegrity and chromatin de-condensation. VitE and T protected germinal cells RNA and protein contents against ATZ-induced damages. CONCLUSION: T and VitE in simultaneous form of administration were able to normalize the ATZ-induced derangements through promoting antioxidant capacity and endocrine function.
ABSTRACT
It has been shown that chronic exposure to cypermethrin (CPM), a pyrethroid pesticide, results in follicular atresia via pathologically affecting angiogenesis, disrupting endocrine potential and enhancing oxidative stress. This study was aimed to uncover the CPM-exposed energy dependent follicular cells apoptosis and to estimate protective effect of vitamin E (VitE) as a potent antioxidant. Thirty six Wistar rats were divided into six groups (n = 6 rats for each group) including; control-sham, CPM-received (CPM, 75 mg kg(-1), intraperitoneally), and CPM and VitE-treated (VitE, 150 mg kg(-1), orally) for 14 and 24 days. The protein biosynthesis of glucose transporter-1 (GLUT-1) and caspase-3 in follicles were estimated by using immuno-histochemical staining at preantral and antral stages. Moreover, the periodic acid Schiff (PAS) staining was performed in order to evaluate the intracytoplasmic carbohydrate ratio in follicular cells and oocyte. Percentages of follicles with GLUT-1, Caspase-3 and PAS-positive cells were compared between groups. Immunohistochemical analyses showed that, VitE significantly up-regulated the GLUT-1 expression and improved the intracytoplasmic carbohydrate supplementation especially at preantral follicles. The cross sections from the CPM-exposed ovaries represented remarkable elevation in percentage of atretic preantral and antral follicles with caspase-3 biosynthesis, which was remarkably (p < 0.05) diminished in VitE co-treated groups. In conclusion, our data showed that VitE by up-regulating of the GLUT-1 biosynthesis improved glucose uptake at follicular cells and oocyte levels that in turn inhibited pro-apoptotic protein caspase-3 biosynthesis.
ABSTRACT
This study aimed to investigate the protective effect of vitamin E (VitE) on cypermethrin (CPM)-induced damages in the ovary. Wistar rats were divided into seven groups (n=6) including; control-sham (c), CPM-received (CPM, 75 mg/kg, i.p.), and CPM and VitE-treated (VitE, 150 mg/kg, orally) for 7, 14 and 24 days. The antioxidant status determination and hormonal assays along with histological and immunofluorescent assessments were performed. The expression of p53 at mRNA level was also examined. The CPM administration affected the ovarian structure and functions as it elevated the follicular atresia and significantly (P<0.05) lowered the estradiol level, time dependently. VitE administration enhanced the CPM-reduced antioxidant capacity, gonadotropins and estradiol levels. Co-administration of VitE and CPM remarkably attenuated the CPM-induced RNA damage in granulosa and theca cells and elevated the deranged angiogenesis. The CPM-reduced micro and macro vessels distribution was significantly (P<0.05) elevated in the VitE-received animals. Expression of p53 at mRNA level was down regulated in the VitE-treated groups completely and relatively following 7 and 14 days, respectively. Our data showed that the CPM-induced biochemical and histological damages could be prevented by VitE. Moreover, protective effects of VitE attribute to its potency in enhancing the antioxidant capacity and promoting the gonadotropins secretion, which resulted in down regulation of p53 overexpression and RNA damage in follicular cells accomplished with improved angiogenesis.