Oxidative stress is considered as a major player in uremia-associated morbidity and mortality in hemodialysis (HD) patients. The aim of this study was to evaluate the effects of turmeric on oxidative stress markers in HD patients. This study was a prospective and double-blind randomized clinical trial. Fifty HD patients aged 18-60 years were recruited after fulfilling the inclusion criteria. Patients were randomly categorized into 2 groups: trial group received turmeric and control group received placebo for 8 weeks. Each patient in the trial group received turmeric, whereas the control group received starch for the same 8 weeks. Plasma malondialdehyde (MDA), red blood cell (RBC) antioxidant enzyme activities as glutathione peroxidase (GPX), glutathione reductase (GR), and catalase (CAT), cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, triglyceride, albumin, and hemoglobin were also measured before and after study. Although MDA level was reduced in both groups, the ratio of decrease was significantly higher in the turmeric group (0.2 vs. 0.1, P = 0.040). Three enzymes of GPX, GR, and CAT levels were increased in both groups; the ratio of increased was significantly higher in the turmeric group for the CAT enzyme (0.73 vs. 0.54; P = 0.02). Also, significant elevation of albumin level in the turmeric group compared with the control group was observed (P = 0.001). Regular ingestion of turmeric reduces plasma MDA and increases RBC CAT activity and plasma albumin levels in HD patients. Turmeric showed no adverse effects.

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Sodium benzoate (SB) is one of the food additives and preservatives that prevent the growth of fungi and bacteria. SB has been shown to improve the symptoms of neurodegenerative disease such as Alzheimer's disease. The aim of this study was to evaluate the effect of SB on the cell survival and cellular antioxidant indices after exposure to aluminum maltolate (Almal) in PC12 cell line as a model of neurotoxicity. The cells exposed to different concentrations of SB (0.125 to 3 mg/mL) in the presence of Almal (500 µM) and cell viability, the level of reactive oxygen species (ROS), glutathione content and catalase activity were measured. The results showed that low concentrations of SB caused an increase in the cell survival, but cell viability was reduced in high concentrations. SB could neither prevent the level of ROS production nor change glutathione content. SB (0.5 mg/mL) significantly increased the catalase enzyme activity as compared to the Almal. This study suggested that SB did not completely protect the cell to aluminum-induced free radicals toxicity. Possibly SB improves the symptoms of neurodegenerative disease by other mechanisms.

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.