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    Bisphenol AF Caused Reproductive Toxicity in Rats and Cineole Co-Treatment Exhibited Protective Effect
    (Springer Heidelberg, 2024) Uyar, Ahmet; Cellat, Mustafa; Kanat, Ozgur; Etyemez, Muhammed; Kutlu, Tuncer; Deveci, Mehmet Zeki Yilmaz; Yavas, Ilker
    Bisphenol AF (BPAF) is increasingly used and now found in products intended for human consumption. The protective effect of 1,8-cineole (CIN) against BPAF-induced reproductive toxicity was investigated. Four groups were created, with each group consisting of eight rats: control, BPAF (200 mg/kg), CIN (200 mg/kg), and BPAF + CIN groups. The results demonstrated that the BPAF group exhibited a decline in testosterone levels and a decrease in sperm parameters compared with the control. Additionally, higher levels of MDA were observed, along with lower levels of GSH and GPx activity. CAT activity also decreased slightly. Tnf-alpha, Nf-kappa B levels were significantly higher, and caspase-3 expression was elevated, while PCNA expression decreased. BPAF significantly increased tissue degeneration compared with the control. However, the BPAF + CIN group showed statistically significant improvements in sperm parameters, except for concentration. They also exhibited an increase in testosterone levels and an improvement in MDA and GSH levels compared with the BPAF group. However, GPx activity partially enhanced. Tnf-alpha and Nf-kappa B levels were significantly reduced, and caspase-3 levels declined while PCNA and Bcl-2 levels increased. The Johnsen Testicular Biopsy score showed a substantial increase. Overall, these results suggest that CIN co-treatment in rats enhanced reproductive health and exhibited antioxidant, antiapoptotic, and anti-inflammatory properties against BPAF-induced testicular damage.
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    Carvacrol showed a curative effect on reproductive toxicity caused by Bisphenol AF via antioxidant, anti-inflammatory and anti-apoptotic properties
    (Pergamon-Elsevier Science Ltd, 2023) Uyar, Ahmet; Cellat, Mustafa; Kanat, Ozgur; Etyemez, Muhammed; Kutlu, Tuncer; Deveci, Mehmet Yilmaz Zeki; Yavas, Ilker
    Bisphenol AF (BPAF) is an endocrine disruptor, and human exposure to these chemicals is growing in industrialized nations. BPAF has been demonstrated in studies to have toxic effects on reproductive health. This study examined the effects of oral exposure to BPAF on the reproductive system and the protective effects of carvacrol in rats. From 32 Wistar albino rats, four separate groups were set up for this purpose. Carvacrol 75 mg/kg and BPAF 200 mg/kg were administered by oral gavage method. Rat sperm parameters and serum testosterone levels were measured after 28 days of administration. The study looked at the MDA in the testis tissues, as well as CAT, GPx, and GSH as antioxidants parameters, NF-& kappa;B and TNF-& alpha; as inflammatory markers, caspase-3 and Bcl-2 as apoptosis parameters, and PCNA as cell proliferation markers. In addition, testis tissues underwent histological evaluation. As a result, in rats exposed to only BPAF, sperm counts declined, testosterone levels reduced, oxidative stress, inflammation, and apoptosis increased, and cell proliferation decreased. Furthermore, severe disruptions in tissue architecture and decreased spermatogenesis were reported. In contrast, sperm parameters improved, testosterone levels increased, oxidative stress and inflammation decreased, and apoptosis was prevented in the carvacrol-treated group compared to the BPAF-only group. It was also found that spermatogenesis was maintained, and structural abnormalities in testicular tissue were mostly avoided with an increase in PCNA expression. According to the findings, despite BPAF-induced testicular and reproductive toxicity, carvacrol had therapeutic potential due to its anti-inflammatory, antioxidant, cell proliferation-increasing, and anti-apoptotic activities.
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    Safranal's therapeutic effects in rat models of polycystic ovary syndrome
    (Springernature, 2024) Cellat, Mustafa; Kuzu, Muslum; Guvenc, Mehmet; Yuksel, Murat; Kanat, Ozgur; Bozkurt, Yesim Akaydin; Etyemez, Muhammed
    Polycystic ovary syndrome is one of the leading causes of female infertility in reproductive age. In this work, the protective effects of safranal against letrozole-induced polycystic ovary syndrome in rats were examined. For this purpose, 32 Wistar albino female rats were split into four groups. Each group received the following treatments for 21 days: Group 1 received carboxymethylcellulose (1%, 2 ml/kg); Group 2, letrozole (1 mg/kg), Group 3, safranal (200 mg/kg); and Group 4 letrozole and safranal via oral gavage. We identified estrus cycles in the rats and analyzed various parameters in their serum and ovarian tissues, as well as histopathologic findings. The parameters studied included C-reactive protein, glucose, total cholesterol, triacylglyceride, high-density lipoprotein, low-density lipoprotein, follicle-stimulating hormone, estradiol, and luteinizing hormone levels in serum. Additionally, the study measured malondialdehyde, glutathione, glutathione peroxidase, and catalase levels in ovarian tissue. We also examined tumor necrosis factor-alpha, interleukin-6, and interleukin-1beta parameters in serum and ovarian tissues, as well as nuclear factor erythroid 2-related factor-2 and heme oxygenase-1 protein levels. In the letrozole group, the estrus cycle was disrupted, and all parameters, except for glutathione and glutathione peroxidase, showed impairments compared to the control group. The findings showed that glucose, triacylglyceride, catalase, and heme oxygenase-1 levels slightly improved after safranal treatment, however, other parameters showed statistically significant improvements. Furthermore, safranal treatment reduced the development of cystic follicles while preserving tissue architecture, as revealed by histopathologic findings. Based on the results obtained, it may be argued that safranal's antioxidant and anti-inflammatory properties, along with its ability to regulate sex hormone levels and manage dyslipidemia, make it a promising solution for patients with polycystic ovary syndrome.