Melatonin ameliorates oxidative damage in hyperglycemia-induced liver injury

Abstract

Purpose: Melatonin (N-acetyl-5-methoxy-tryptamine) is synthesized mainly by the pineal gland and its antioxidant properties have been demonstrated both in short and long term studies. Our aim was to clarify the e ects of hyperglycemia and to administer melatonin on lipid peroxidation, protein oxidation and oxidative DNA damage in rat.Methods: Malondialdehyde (MDA), protein carbonyl (PCO) and total thiol (T-SH) levels were determined in plasma and liver tissue, glutathione (GSH) levels in erythrocyte and liver tissue, and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in plasma and liver.irty-eight male Wistar rats were divided into four groups: 1 -injected with saline (n = 8), 2 -injected with melatonin (n = 10), 3 -injected with STZ (65 mg/kg, i.p.) (diabetic group) (n = 10) and 4 -injected with melatonin (10 mg/kg/day, i.p.) and STZ (65 mg/kg, i.p.) (n = 10) for 8 weeks (diabetic+ melatonin group). Colorimetric methods were used to determine the level of the oxidative stress markers. 8-OhdGwas measured using ELISA.Results: MDA, PCO and 8-OHdG levels in the plasma and the liver homogenates of diabetic rats were higher than controls and were signi cantly reduced a er melatonin treatment. T-SH and GSH levels in samples were markedly reduced in untreated diabetic rats compared with control rats; however, these parameters were increased in diabetic rats following melatonin treatment. Conclusion:Our ndings showed that melatonin administration partially ameliorated oxidative damage in liver injury in STZ-induced diabetic rats. e present study suggests that melatonin functions as a potent antioxidant agent in diabetes. Melatonin, a nutritional supplement, may be a good therapeutic option for diabetic patients.

Fluorimetric screening assay for protein carbonyl evaluation in biological samples

“…The carbonyl levels (in nmol/mg protein) determined in plasma (0.75 ± 0.09) and liver homogenates (1.85 ± 0.11) from control rats using the NBDH assay (Fig. 6) are in good agreement with much reported data of PC contents obtained by other techniques [36][37][38][39][40]. When the protein oxidative damage was investigated in the STZ-diabetic group with the two methods, a significant increase in PC values (1.8-and 1.3-fold in plasma and liver samples, respectively) was indicated as compared with normal control rats (Fig.…”

“…These divergences between baseline absolute values were attributed to differences in the standardization procedures [38]. However, despite the baseline values being found different in control animals, an approximately 2-fold increase in these PC values after STZ treatment was found in all studies despite some differences that could exist in the STZ doses or postinjection period duration [39][40][41].…”

“…Before PC analysis, it was checked whether all rats of the STZ-diabetic group had developed diabetes within the 4 weeks after STZ injection, as indicated by increased blood glucose concentrations (494 ± 21 mg dl À1 in STZ-diabetic rats vs. 78 ± 3 mg dl À1 in controls, P < 0.01) and loss of body weight (258 ± 9 g in STZ-diabetic rats vs. 353 ± 15 mg in controls, P < 0.05). Some discrepancies in the plasmatic PC absolute values of normal animals were found in the literature, with a large range from 1 to 17 nmol/mg protein [36][37][38][39][40][41]. These divergences between baseline absolute values were attributed to differences in the standardization procedures [38].…”

Diyabetik Sıçanlarda Melatonin Uygulamasının Karaciğer, Böbrek, Mide, Pankreas ve Göz Dokularında Oksidatif Stres Üzerine Etkisi

“…Ancak melatonin tedavisi sonrasında MDA düzeylerinde istatistiksel olarak anlamlı bir azalma olmazken, GSH düzeylerinin diyabet+SF grubuna göre anlamlı olarak arttığı saptandı. GSH düzeylerindeki bu değişim literatürle uyumludur (22,25). Bizim çalışmamızda diyabetik sıçanlarda melatonin uygulamasının lipid peroksidasyonu üzerine etkili olmaması çeşitli nedenlerden dolayı olabilir.…”

Impact of melatonin on immunity: a review

“…Melatonin would be a suitable tool for resolving of the results of oxidative insult. Some studies on that issue have been done: the beneficial effects include amelioration of hyperglycemia-induced liver injury [45], reduction of hypoxia induced pathologies [46] and reduction of poisoning with chlorpyrifos [47]. Despite the promising findings, there is a long path before melatonin can be reasonably used for treatment of the pathologies: there is no known molecular mechanism that describes both the pathology and the melatonin-based therapy.…”