Browsing by Author "Yavas, Mehmet Cihan"

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Citation - Scopus: 1
Determination of the Protective Effect of Curcumin Against Tartrazine-Induced DNA Damage and HSP 70 in the Rat Brain
(Springer, 2025) Yavas, Mehmet Cihan; Tan, Fazile Canturk; Tur, Kardelen; Keskin, Cumali; Basmaci, Guldidar
Tartrazine is a widely used food dye, and children often consume large amounts of food products containing this additive due to their appealing appearance. Curcumin, on the other hand, is known for its antioxidant properties. The aim of this study was to investigate the protective effects of curcumin on brain tissue and biochemical parameters in rats exposed to short-term tartrazine administration. Male Wistar albino rats were randomly divided into five equal groups. Group 1 served as the control; Group 2 received tartrazine (10 mg/kg); Group 3 received tartrazine (100 mg/kg); Group 4 received tartrazine (10 mg/kg) along with curcumin (20 mg/kg); and Group 5 received tartrazine (100 mg/kg) along with curcumin (20 mg/kg). All substances were administered via oral gavage. The study lasted for 21 days. Serum samples were analyzed for heat shock protein 70 (HSP70) levels using the ELISA method. Brain tissues were subjected to histopathological examination and DNA damage assessment using the comet assay. Although HSP70 levels increased in the tartrazine groups, the differences were not statistically significant (p = 0.065). Partial damage was observed in the histopathological analysis. Comet assay results indicated a dose-dependent increase in DNA tail percentage with tartrazine, which was reduced following curcumin administration. These findings suggest that curcumin may alleviate tartrazine-induced damage in brain tissue and may have a regulatory effect on serum HSP70 levels in rats.
Diethyl Phthalate-Induced Oxidative Stress, Genotoxicity, and Thyroid Hormone Disruption in Female Wistar Rats
(Pergamon-Elsevier Science Ltd, 2026) Komurcu, Ayse; Yavas, Mehmet Cihan
Background: Diethyl phthalate (DEP), a common plasticizer in cosmetics and personal care products, is known to induce oxidative stress and endocrine disruption. Its widespread use raises concerns about thyroid toxicity. Objective: This study aimed to evaluate the genotoxic and endocrine effects of subacute DEP exposure on thyroid tissue in female Wistar albino rats using thyroid hormones, oxidative stress markers, DNA damage, and histopathology. Methods: Twenty-eight female Wistar albino rats were divided into four groups (n = 7): control, 100 mg/kg, 300 mg/kg, and 600 mg/kg DEP. DEP was administered orally for 21 days. DNA damage was assessed by Comet Assay, oxidative stress markers (TAS, TOS, OSI) were measured, and serum TSH, T3, and T4 levels were determined by ELISA. Body weights were monitored, and thyroid tissues were examined histologically. Results: Compared to the control group, T3 and T4 levels decreased (P < 0.05), TSH levels increased (p < 0.05), TAS levels decreased (p < 0.05), and TOS and OSI levels increased (p < 0.05). Comet Assay showed dose-dependent DNA damage (tail DNA%, p < 0.05). With higher DEP doses, thyroid tissue histopathology changed significantly. Conclusion: Subacute DEP exposure causes dose-dependent genotoxicity, oxidative stress, and endocrine disruption in thyroid tissue. These findings emphasize the need to limit environmental and human DEP exposure.
Dose-Dependent Hepatotoxicity of Diethyl Phthalate in Female Wistar Rats
(MDPI, 2026) Tan, Fazile Canturk; Gokdemir, Gul Sahika; Kalkan, Kubra Tugce; Varol, Salih; Yavas, Mehmet Cihan; Cantürk Tan, Fazile
Phthalates are a class of compounds commonly used as plasticizers in various industrial and consumer products. In line with the increasing environmental and biological exposure concerns regarding these compounds, this study investigated the dose-dependent effects of diethyl phthalate (DEP) on the liver in a subacute rat model. Diethyl phthalate (DEP) was given orally by gavage to female Wistar albino rats at doses of 100, 300, and 600 mg/kg body weight per day for 21 days in order to assess liver tissue and associated function test levels. Liver function was evaluated by analyzing serum biochemical data. Liver tissues were evaluated using histopathological staining (H&E and Masson's trichrome staining), immunohistochemical analysis of IL-1 beta and TGF-beta, tissue ELISA for IL-6 and TNF-alpha, and comet assay to determine DNA damage. DEP exposure was found to cause significant, dose-dependent histopathological changes in liver tissue, including hepatocyte necrosis, cytoplasmic vacuolization, sinusoidal dilation, and vascular congestion. AST levels were significantly increased compared to the control group, while no significant changes were observed in other serum biochemical parameters. Compared to the control group, the expression of pro-inflammatory cytokines (IL-6 and TNF-alpha), IL-1 beta, and TGF-beta was found to be elevated in the DEP-treated groups, and their levels increased with increasing exposure dose. DEP exposure also caused significant DNA damage in liver tissue. These findings indicate that despite an increase in AST levels observed in subacute DEP exposure, there were limited changes in serum biochemical parameters; serum liver enzymes alone may not fully reflect the extent of hepatic damage, and DEP can cause significant inflammatory, histopathological, and genotoxic effects in liver tissue.
Toxic Effects of Tartrazine and the Protective Role of Curcumin on Liver Function and DNA Integrity in Male Rats
(Wiley, 2025) Varli, Metin; Yavas, Mehmet Cihan; Canturk Tan, Fazile; Tur, Kardelen; Basmaci, Guldidar
Tartrazine (TAR) and curcumin (CUR) are commonly utilized in the food manufacturing sector. The present investigation was designed to assess the hepatotoxic impact of the food dye tartrazine on hepatic function and its related biomarkers. We systematically allocated 35 male Wistar rats into five homogeneous groups. The specified groups consisted of: control, TAR at a dosage of 10 mg/kg/day, TAR at a dosage of 100 mg/kg/day, TAR at a dosage of 10 mg/kg/day combined with CUR at 20 mg/kg/day, and TAR at a dosage of 100 mg/kg/day combined with CUR at 20 mg/kg/day. All experimental groups received the treatment via oral gavage. Our findings indicated that as the TAR dosage escalated relative to the control group, the levels of superoxide dismutase (SOD), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT) exhibited an increase, while the alpha-fetoprotein (AFP) level demonstrated a decline. In the CUR-treated groups, in comparison with the control groups, the levels of SOD, AST, ALT, LDH, total bilirubin, GGT, and AFP increased in the low-dose TAR groups, whereas ALP levels decreased. Our histopathological analysis disclosed the occurrence of degenerative changes in both TAR and CUR treatment groups. The genotoxic assessment, utilizing the DNA comet assay, revealed that an increase in TAR dosage corresponded with heightened DNA damage; however, the incorporation of CUR mitigated this detrimental effect. Our findings suggest that tartrazine may exert deleterious effects on hepatic function, whereas curcumin has displayed partial therapeutic efficacy.