Efficacy of melatonin in restoring the antioxidant status in the lens of diabetic rats induced by streptozotocin

Abstract

Background Melatonin is a well-known free radical scavenger. The present study aimed to investigate the effects of melatonin treatment on the antioxidant status in the lenticular tissue of streptozotocin (STZ)-induced diabetic rats. Methods Thirty-four male rats were randomly divided into four groups as follows: healthy control rats (group 1, n = 10); diabetic control rats (group 2, n = 10); melatonin-treated (5 mg/kg•day) diabetic rats (group 3, n = 10) and melatonin-treated (5 mg/kg• day) healthy rats (group 4, n = 4). Diabetes was induced by injection of streptozotocin (50 mg/kg, ip). Following 8-weeks of melatonin treatment, all rats were killed and the blood plasma and their lenses were stored at −70°C for antioxidant enzyme activities assay and biochemical determination. Results The plasma glucose and lens malondialdehyde (MDA) increased significantly in the rats of group 2 as compared to the group 1. Also, a significant decrease in the levels of catalase (CAT) and glutathione reductase (GR) activities in the lenses and plasma reduced glutathione (GSH) was found. However, the levels of lenticular MDA (not significant) and the plasma glucose significantly decreased in the rats of group 3 compared to the group 2. Besides, the levels of CAT, GR in the rats lens and plasma GSH increased significantly. Conclusion Diabetes mellitus induced hyperglycemia and oxidative stress, whereas melatonin decreased the blood glucose levels and lipid peroxidation and increased the activities of antioxidant enzymes in diabetic rat lenses.

Melatonin prevents deterioration of erectile function in streptozotocin‐induced diabetic rats via sirtuin‐1 expression

“…After the first week, the blood glucose levels of the rats that were treated with insulin, melatonin, or a combination of the two agents seemed to return to those of the controls. Interestingly, melatonin was found to regulate the blood glucose levels in a manner similar to that observed for insulin therapy in earlier studies (Andersson & Sandler, 2001; Khorsand, Akmali, & Akhzari, 2019; Montilla et al., 1998). The increase in the MDA and 8‐OHdG levels and caspase‐3 activity, in addition to the concomitant decrease in the cGMP levels and NOS activity, suggested the presence of hyperglycemia‐induced oxidative stress on the CC.…”

Melatonin alleviates cardiac fibrosis via inhibiting lncRNA MALAT1/miR‐141‐mediated NLRP3 inflammasome and TGF‐β1/Smads signaling in diabetic cardiomyopathy

“…Some studies reported that melatonin improves insulin sensitivity, increases insulin secretion and prevents hyperglycemia. [43][44][45] However, others showed that melatonin treatment does not significantly affect the blood glucose in diabetic animals, but can still alleviate diabetic cardiac dysfunction through preventing mitochondrial fission, reducing myocardial oxidative stress, inducing cardiac autophagy and limiting myocardial apoptosis. 19,20,36,38,46 Moreover, the recently published results from highly cited prospective randomized clinical trials failed to demonstrate improvement of cardiovascular prognosis with aggressive glycemic control.…”

“…Nevertheless, this issue has been controversial. Some studies reported that melatonin improves insulin sensitivity, increases insulin secretion and prevents hyperglycemia . However, others showed that melatonin treatment does not significantly affect the blood glucose in diabetic animals, but can still alleviate diabetic cardiac dysfunction through preventing mitochondrial fission, reducing myocardial oxidative stress, inducing cardiac autophagy and limiting myocardial apoptosis .…”

Impact of Antioxidants on Pancreatic B-Cell Damage Caused by Streptozotocin in Adult Male Albino Rats

“…A marker of oxidative stress, serum GSH, was reported to be lowered by streptozotocin treatment [12] . The MDA in the untreated streptozotocin rat increased dramatically [13] , and the GSH activity significantly decreased in comparison to the control groups [14] . Improvement in pancreatic structure was evident in group V, possibly as a result of vitamin E's antioxidant properties, which reduce oxidative stress and shield pancreatic cells from the creation of free radicals while promoting cellular regeneration and proliferation [15] .…”