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- MakaleYalnız künye2025Scopus SJRQ1Naringenin Attenuates Testicular Toxicity and Apoptosis in Rats Chronically Exposed to Mercury Chloride
Kahramanoğullari, Merve; Erişir, Mine; Yaman, Mine; Kaya, Şeyma Özer; Ak, Tuba Parlak
Mercury is an industrial toxin with detrimental effects on the reproductive system. This study explored the impact of naringenin (NAR) on testicular toxicity and apoptosis in rats chronically exposed to mercury chloride (MC). The research involved 41 adult male Wistar-Albino rats aged about 2.5 months, which were allocated into 5 groups: group 1 was a control group, group 2 received 100mg/kg of NAR, group 3 was exposed to MC, group 4 received both MC and 50mg/kg of NAR, and group 5 received both MC and 100mg/kg of NAR. For the treatments, the control group took 1mL/kg saline via intraperitoneal (ip) injection and 1mL/kg corn oil via gavage. MC was administered at 0.4mg/kg/day to the MC groups via ip, and NAR was delivered in corn oil at 50 and 100mg/kg/day to the respective NAR groups via gavage. All treatments were performed over a period of 20 days, with MC administration starting 1 hour after NAR administration. The irregularity and loss in spermatogenic cell organization, degeneration and vacuolization in tubules, edema, and congestion in interstitial areas of the testicular tissue of the MC group were alleviated by NAR administration. In addition, the increase in Caspase 3, iNOS, and eNOS immunoreactivities of the MC group were alleviated by NAR administration. In conclusion, it was found that NAR had protective and therapeutic effects against oxidative damage, histopathological changes, apoptosis, and altered spermatological parameters resulting from MC exposure in the testis, and 100mg/kg NAR provided positive effects on altered histopathological analysis, spermatological parameters, and apoptosis.
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İncele - MakaleAçık Erişim2024Scopus SJRQ2Effects of naringenin on oxidative damage and apoptosis in liver and kidney in rats subjected to chronic mercury chloride
Kahramanoğullari, Merve; Erişir, Mine; Yaman, Mine; Parlak Ak, Tuba
Mercury chloride is a type of heavy metal that causes the formation of free radicals, causing hepatotoxicity, nephrotoxicity and apoptosis. In this study, the effects of naringenin on oxidative stress and apoptosis in the liver and kidney of rats exposed to mercury chloride were investigated. In the study, 41 2-month-old male Wistar-Albino rats were divided into five groups. Accordingly, group 1 was set as control group, group 2 as naringenin-100, group 3 as mercury chloride, group 4 as mercury chloride + naringenin-50, and group 5 as mercury chloride + naringenin-100. For the interventions, 1 mL/kg saline was administered to the control, 0.4 mg/kg/day mercury (II) chloride to the mercury chloride groups by i.p., and 50 and 100 mg/kg/day naringenin prepared in corn oil to the naringenin groups by gavage. All the interventions lasted for 20 days. Mercury chloride administration was initiated 1 h following the administration of naringenin. When mercury chloride and the control group were compared, a significant increase in plasma urea, liver and kidney malondialdehyde (MDA) levels, in kidney superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) activities (p <.001), and a significant decrease in liver and kidney glutathione (GSH) levels (p <.001), in liver catalase (CAT) activity (p <.01) were observed. In addition, histopathological changes and a significant increase in caspase-3 levels were detected (p <.05). When mercury chloride and treatment groups were compared, the administration of naringenin caused a decrease aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH) (p <.01), urea, creatinine levels (p <.001) in plasma, MDA levels in liver and kidney, SOD, GSH-Px, GST activities in kidney (p <.001), and increased GSH levels in liver and kidney. The addition of naringenin-100 increased GSH levels above the control (p <.001). The administration of naringenin was also decreased histopathological changes and caspase-3 levels (p <.05). Accordingly, it was determined that naringenin is protective and therapeutic against mercury chloride-induced oxidative damage and apoptosis in the liver and kidney, and 100 mg/kg naringenin is more effective in preventing histopathological changes and apoptosis.
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İncele - MakaleYalnız künye2021Scopus SJRQ2Chrysin protects against testicular toxicity caused by lead acetate in rats with its antioxidant, anti-inflammatory, and antiapoptotic properties
Ileriturk, Mustafa; Benzer, Fulya; Aksu, Emrah Hicazi; Yildirim, Serkan; Kandemir, Fatih Mehmet; Dogan, Tuba; Dortbudak, Muhammet Bahaeddin; Genc, Aydin
In the present study, the protective effects of chrysin (CHR) against testicular damage caused by lead acetate (PbAc) were examined. In this way, 30 min after rats were given 25 and 50 mg/kg/b.w CHR orally for seven consecutive days, 30 mg/kg/b.w PbAc was administered orally. In biochemical analysis of testicular tissue, it was found that PbAc-reduced antioxidant parameters [glutathione peroxidase (GPx), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)], while it increased lipid peroxidation, inflammatory markers [nuclear factor kappa-B (NF-κB), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE-2), and inducible nitric oxide synthase (iNOS)], and 8-hydroxy-2′-deoxyguanosine (8-OHdG). In the immunohistochemical examination, it was determined that PbAc increased the expression of tumor necrosis factor-α (TNF-α) and caspase-3. Accordingly, PbAc was found to cause a decrease in sperm motility and an increase in the percentage of dead sperm. However, it has been observed that CHR relieves oxidative stress due to its antioxidant properties, thus protecting against inflammation and apoptosis. It also allowed the CHR sperm parameters to return to control group levels. The results revealed that CHR could be a natural substance to be used in Pb-induced testicular toxicity. Practical applications: Lead (Pb) is an important environmental contaminant heavy metal. Pb is believed to reduce fertility in men. Oxidative stress plays a significant role in the damage caused by Pb to testicular tissue. CHR is an antioxidant substance that occurs naturally in various plants and has various pharmacological properties. In the present study, it was investigated whether CHR has a protective effect against testicular toxicity induced by PbAc. The results revealed that in rats, CHR protects the testicular tissue from PbAc toxicity by showing antioxidant, anti-inflammatory and anti-apoptotic effects, thus bringing sperm parameters closer to normal.
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