DNA protective and antioxidative effects of melatonin in streptozotocin-induced diabetic rats

The study results indicate that the intraperitoneal administration of 10 mg/kg MEL over 6 weeks may cause amelioration in oxidative stress parameters against diabetes, leading to beneficial effects based on % tail DNA and mean tail moment parameters in rat lymphocytes.

📌 3 Key Takeaways

🎯

Objective & Hypothesis:Diabetes mellitus is a chronic disease characterized by elevated blood sugar levels.

📊

Key Findings & Data:In total, 32 rats were equally divided into four experimental groups: control, melatonin, diabetic, and diabetic + melatonin.

💡

Conclusion & Impact:The study results indicate that the intraperitoneal administration of 10 mg/kg MEL over 6 weeks may cause amelioration in oxidative stress parameters against diabetes, leading to beneficial effects based on % tail DNA and mean tail moment parameters in rat lymphocytes.

🔬Design:Research Article

📍Scope:Comprehensive Sample

⚙️Variables:Diabetes mellitus · comet assay · oxidative stress

Abstract

Diabetes mellitus is a chronic disease characterized by elevated blood sugar levels. In diabetic patients, oxidative stress induced by the presence of excessive free radicals is closely associated with chronic in?ammation, leading to potential tissue damage. Melatonin (MEL) is a compound synthesized by the pineal gland and a scavenger of free radicals. The aim of this study was to research the effects of MEL on oxidative stress and its DNA protective effects in streptozotocin-induced diabetic rats. In total, 32 rats were equally divided into four experimental groups: control, melatonin, diabetic, and diabetic + melatonin. A single dose of streptozotocin (60 mg/kg) was given by intraperitoneal route to induce experimental diabetes. MEL (10 mg/kg daily) was administrated to rats by intraperitoneal route for 6 weeks. Oxidative stress parameters were evaluated in rat liver, kidney, brain, and pancreas tissues. Body weight, plasma glucose, and HbA1c levels were studied. DNA damage was analyzed by comet assay in lymphocytes, while % tail DNA and mean tail moment parameters were evaluated. The study results indicate that the intraperitoneal administration of 10 mg/kg MEL over 6 weeks may cause amelioration in oxidative stress parameters against diabetes, leading to beneficial effects based on % tail DNA and mean tail moment parameters in rat lymphocytes.

Özet

Diabetes mellitus is a chronic disease characterized by elevated blood sugar levels. In diabetic patients, oxidative stress induced by the presence of excessive free radicals is closely associated with chronic in?ammation, leading to potential tissue damage. Melatonin (MEL) is a compound synthesized by the pineal gland and a scavenger of free radicals. The aim of this study was to research the effects of MEL on oxidative stress and its DNA protective effects in streptozotocin-induced diabetic rats. In total, 32 rats were equally divided into four experimental groups: control, melatonin, diabetic, and diabetic + melatonin. A single dose of streptozotocin (60 mg/kg) was given by intraperitoneal route to induce experimental diabetes. MEL (10 mg/kg daily) was administrated to rats by intraperitoneal route for 6 weeks. Oxidative stress parameters were evaluated in rat liver, kidney, brain, and pancreas tissues. Body weight, plasma glucose, and HbA1c levels were studied. DNA damage was analyzed by comet assay in lymphocytes, while % tail DNA and mean tail moment parameters were evaluated. The study results indicate that the intraperitoneal administration of 10 mg/kg MEL over 6 weeks may cause amelioration in oxidative stress parameters against diabetes, leading to beneficial effects based on % tail DNA and mean tail moment parameters in rat lymphocytes.

Keywords

Diabetes mellitus comet assay oxidative stress melatonin streptozotocin DNA damage MDA level tail moment % tail DNA DNA repair

🔖

Cite This Article

SEKKİN, S., İPEK, E. D., BOYACIOĞLU, M., KUM, C., KARADEMİR, Ü., YALINKILINÇ, H. S., AK, M. O., BAŞALOĞLU, H. (2015). DNA protective and antioxidative effects of melatonin in streptozotocin-induced diabetic rats. Turkish Journal of Biology, Cilt: 39 - Sayı: 6, 932–940. https://ajindex.com/articles/181588

📄 Full Text PDF Viewer

Open in New Tab ↗

↗New Tab

📄

PDF görüntüleyici hazırlanıyor...

References (11)

Aebi H (1984). Catalase in vitro assay methods. Methods Enzymol 105: 121–126.
Agil A, Reiter RJ, Jimenez-Aranda A, Iban-Arias R, Navarro-Alarcon M, Marchal JA, Adem A, Fernandez-Vazquez G (2013). Melatonin ameliorates low-grade inflammation and oxidative stress in young Zucker diabetic fatty rats. J Pineal Res 54: 381– 388. Aksoy N, Vural H, Sabuncu T, Aksoy S (2003). Effects of melatonin on oxidative-antioxidative status of tissues in streptozotocin- induced diabetic rats. Cell Biochem Funct 21: 121–125.
Andersson AK, Sandler S (2001). Melatonin protects against streptozotocin, but not interleukin-1β-induced damage of rodent pancreatic beta-cells. J Pineal Res 30: 157–165.
Arif M, Islam MR, Waise TM, Hassan F, Mondal SI, Kabir Y (2010). DNA damage and plasma antioxidant indices in Bangladeshi type 2 diabetic patients. Diabetes Metab 36: 51–57.
Bibak B, Khalili M, Rajaei Z, Soukhtanloo M, Hadjzadeh MA, Hayatdavoudi P (2014). Effects of melatonin on biochemical factors and food and water consumption in diabetic rats. Adv Biomed Res 3: 173. Brownlee M (2005). The pathobiology of diabetic complications: a unifying mechanism. Diabetes 54: 1615–1625.
Cam M, Yavuz O, Guven A, Ercan F, Bukan N, Ustundag N (2003). Protective effects of chronic melatonin treatment against kidney injury in streptozotocin-induced diabetic rats. J Pineal Res 35: 212–220. Carpentieri A, de Barboza GD, Areco V, López MP, de Talamoni NT (2012). New perspectives in melatonin uses. Pharmacol Res 65: 437–444.
Cemeli E, Baumgartner A, Anderson D (2009). Antioxidants and the Comet assay. Mutat Res 681: 51–67.
Collins A, Dušinská M, Franklin M, Somorovská M, Petrovská H, Duthie S, Fillion L, Panayiotidis M, Rašlová K, Vaughan N (1997). Comet assay in human biomonitoring studies: Reliability, validation, and applications. Environ Mol Mutagen 30: 139–146.
Collins AR (2014). Measuring oxidative damage to DNA and its repair with the comet assay. Biochim Biophys Acta 1840: 794– 800. Dalle-Donne I, Rossi R, Colombo R, Giustarini D, Milzani A (2006). Biomarkers of oxidative damage in human disease. Clin Chem 52: 601–623.
Dhawan A, Bajpayee M, Parmar D (2009). Comet assay: a reliable tool for the assessment of DNA damage in different models. Cell Biol Toxicol 25: 5–32.
Di Naso FC, Simoes Dias A, Porawski M, Marroni NA (2011). Exogenous superoxide dismutase: action on liver oxidative stress in animals with streptozotocin-induced diabetes. Exp Diabetes Res 2011: 754132. Elbe H, Vardi N, Esrefoglu M, Ate