Decline of estrogen during menopause has been associated with numerous significant changes that have been linked to many pathophysiological complications. In addition, ovarian hormone deficiency increases the production of reactive oxygen radicals which could result in oxidative stress and cell damage. While estrogen therapy is often considered to overcome the behavioral and physiological shortcomings, antioxidants are gaining popularity for their beneficial property. For this purpose, in the present study, utilizing the antioxidant properties of beta glucan has been examined in treatment of menopause induced oxidative stress in cerebral neurons. Four groups of female Wistar rats were used: control, ovariectomy, ovariectomy + estrogen treated and ovariectomy + beta glucan treated. We observed a significant increase in neural degeneration in ovariectomized rats as compared to controls. Moreover, increased oxidative stress in the brains of the ovariectomized rats has been detected by performing immunohistochemical analysis. A large number of immuno-positive cerebral neurons have been observed in ovariectomy group rat brains. Interestingly, providing beta glucan treatment to ovariectomized rats reduced the number of degenerated neurons. Our study is the first to examine light and electron microscopic examination and immunohistochemical and stereological analysis of estrogen depletion in rats and to test protective role of beta glucan in the experimental study.

Objectives: Menopause has a negative effect on cardiovascular functions. However, very little is known of the overall effect of menopause on the cardiac ultrastructure or the pathophysiological basis of this. Methods: A group of 12-week-old female Sprague Dawley rats were randomly allocated to healthy control (n = 6) and ovariectomy groups (n = 6). Twelve weeks after ovariectomy, the rats’ cardiac tissues were histopathologically analyzed for determination of oxidant and antioxidant enzymes [activities of catalase (CAT), superoxide dismutase (SOD), and myeloperoxidase (MPO) and amount of glutathione (GSH) and lipid peroxidation (LPO)]. Results: When compared to the control group, the ovariectomy group showed cardiomyopathic changes. In tissue, activities of CAT (185 ± 2.4 vs. 112 ± 1.4 mmol/min/mg tissue; p < 0.05), SOD (153 ± 1.0 vs. 146 ± 0.7 mmol/min/mg tissue; p < 0.05) and MPO (19 ± 0.8 vs. 8.6 ± 0.11 µmol/min/mg tissue; p < 0.05) and LPO levels (32.1 ± 0.77 vs. 14.4 ± 0.20 nmol/g tissue; p < 0.05) were significantly increased in the ovariectomy group when compared to the control group. However, GSH levels (3.43 ± 0.02 vs. 3.73 ± 0.01 nmol/g tissue; p < 0.05) were significantly lower in the ovariectomy group when compared to the control group. Conclusion: Using an experimental animal model, we were able to demonstrate that menopause causes cardiomyopathic changes, and we propose that these changes could be mediated by oxidative stress.

Background: The present study investigated the protective effects of carvacrol (CAR) against testicular toxicity induced by sodium arsenite (SA).Methods and Results: Rats were given SA and/or CAR for 14 days. Semen analyzes showed that CAR increased sperm motility and decreased the percentage of anarmol and dead sperm. It was determined that the oxidative stress induced by SA decreased with the increase of Nrf-2 and HO-1 expressions, SOD, CAT, GPx and GSH levels, and MDA levels decreased after CAR treatment. It was observed that autophagy and in ammation triggered by SA in testicular tissue were alleviated by suppressing the expressions of LC3A, LC3B, MAPK-14, NF-kB, TNF-a, IL-1b, iNOS and COX-2 biomarkers in rats given CAR. CAR treatment protected against apoptosis by suppressing Bax and Caspase-3 expressions and triggering Bcl-2 expression in testicles.Conclusions: As a result, it was seen that CAR could provide protection against SA-induced damage in testicular tissues of rats.

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We aimed to determine the possible effects of the antioxidant agent (1 → 3)‐β‐D‐glucan on bortezomib‐induced rat testis damage. We used five groups of rats; control, (1 → 3)‐β‐D‐glucan (75 mg/kg), bortezomib group, bortezomib + (1 → 3)‐β‐D‐glucan groups (injection of (1 → 3)‐β‐D‐glucan after bortezomib and sacrificed at 48th or 72nd h). The effects of these substances were assessed by measuring the levels of the antioxidant enzymes and LPO, and by performing immunohistochemical analysis with NF‐κB. The histology of testis was evaluated using aniline blue staining. (1 → 3)‐β‐D‐glucan leads to significant reductions in the levels of antioxidant enzymes and increased levels of LPO in testes. Moreover, it increased the NF‐κB immunopositivity significantly in testis, especially in Bortezomib + (1 → 3)‐β‐D‐glucan group at 48th h. The histological changes were observed in the bortezomib and/or (1 → 3)‐β‐D‐glucan groups. Our results demonstrated that testis damage caused by the treatment with bortezomib was not eliminated by (1 → 3)‐β‐D‐glucan and shockingly it increased the damage. Practical applications The testis damage caused by the treatment with bortezomib was not eliminated by (1 → 3)‐β‐D‐glucan and as a result, β‐1,3‐(D)‐glucan enhanced the toxicity by leading a decrease in the levels of GSH, SOD, and CAT, thus caused an elevation in the immunoreactivity of NF‐κB and altered the histopathological changes by enhancing the toxic effects of bortezomib. The findings of the previous studies about the antioxidative activity of (1 → 3)‐β‐D‐glucan are controversial. So, it is necessary to consider the cytotoxicity of (1 → 3)‐β‐D‐glucan in testis tissue. Thus, more studies on testis tissue are necessary to confirm that (1 → 3)‐β‐D‐glucan is safe as an antioxidant.