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Comparative Study 2006; 27(5): 631-638 PubMed PMID: 17159829 Citation  Keywords:  Animals, Body Weight:drug effects, Diet:adverse effects, Glutathione Peroxidase:metabolism, Goiter:blood, Iodine:urine, Male, Organ Size:drug effects, Potassium Iodide:administration & dosage, Rats, Rats, Wistar, Selenium:deficiency, Thyroid Gland:drug ef.   

OBJECTIVE: A possible link was proposed between selenium [Se(-)], iodine deficiency and thyroid pathology. The aim of the study was to examine changes in FT3 and FT4 concentrations, weights of the thyroid glands and ioduria after potassium iodide (KI) in normal and goitrogenic rats on Se(-) diet.

METHODS: Wistar rats in Group 1 received the standard diet. Other animals remained (3 months) either on a Se(-) diet alone [Groups 2-5] or supplemented with selenium [Se(+)] (Group 6-8). After 9 weeks, Groups 3, 4, 6, 7 received sodium perchlorate [I(-); 1 month]. KI (1 mg/rat) was injected in Groups 4, 5, 7, 8. The animals were decapitated 3 days after the injections.

RESULTS: FT4 was higher in serum of Se(-) rats than in that of Se(+). The differences of FT3 were not statistically significant. In I(-) Groups, the levels of FT3 and FT4 were very low. KI increased both thyroid hormones in I(-) rats but the effect was especially pronounced for FT3. KI decreased the weights of the glands, enlarged in the I(-) animals, both on Se(-) and Se(+) diet. Urine iodide concentrations were lower in Se(-) animals; KI increased ioduria.

CONCLUSIONS: These data demonstrate that selenium and iodine deficiencies may play an essential role in thyroid hormone metabolism....

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Comparative Study 2006; 27(3): 365-368 PubMed PMID: 16816830 Citation  Keywords:  Animals, Female, Glutathione:metabolism, Glutathione Peroxidase:metabolism, Glutathione Transferase:metabolism, Kidney:enzymology, Liver:enzymology, Male, Melatonin:physiology, Mice, Random Allocation,.   

OBJECTIVES: The changes in reduced glutathione (GSH), activity of glutathione transferase (GST) and glutathione peroxidase (GSPx) after administration of exogenous melatonin (N-acetyl-5-methoxy-tryptamine) at a dose 20 mg/kg b.w. were investigated for five and ten days in the liver and kidney of male and female mice.

METHODS: The liver and kidney were homogenized in 0.1 M phosphate buffer. Glutathione level and activity of studied glutathione enzymes were determined in the supernatants.

RESULTS: Melatonin caused an increase in glutathione level, the activity of glutathione peroxidase as well as glutathione transferase in the examined organs.

CONCLUSION: Melatonin may exert some effects on the activity of enzymes engaged in the metabolism of thiol compounds in the cell. Glutathione may be useful for monitoring melatonin's protective role on cell damage....

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Journal Article 2005; 26(4): 419-422 PubMed PMID: 16135998 Citation  Keywords:  Animals, Antibiotics, Antineoplastic:pharmacology, Antioxidants:pharmacology, Blood Glucose, Carnitine:pharmacology, Diabetes Mellitus, Experimental:metabolism, Drug Interactions, Glutathione Peroxidase:metabolism, Male, Rats, Rats, Wistar, Streptozocin:p.   

OBJECTIVES: L-carnitine is a naturally compound widely distributed in the body. It has an antiradical effect and decreases lipid peroxidation. In acute or chronic streptozotocin (STZ)-induced diabetic rats, the pancreatic content of carnitine was found to be significantly lower than nondiabetic group. We investigated the effects of L-carnitine on the development of STZ-induced diabetes in rats, to determine if L-carnitine can prevent the onset of diabetes or reduce the severity of hyperglycemia and this prevention/reduction is associated with the reduction in oxidative stress.

SETTING AND DESIGN: The rats were divided into 3 groups: Control, STZ-treated (65 mg/kg intraperitoneally) and L-carnitine (500 mg/kg) and STZ-treated.

METHODS: Oxidative stress was assessed by measuring pancreatic thiobarbituric acid reactive substance (TBARS) formation levels using the method of Rehncrona et al, pancreatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities using a Randox test combination (RANSOD and RANDOX).

RESULTS: L-carnitine did not prevent the onset of diabetes at this dose. Development of diabetes was associated with an increase in pancreatic TBARS (0.028 +/- 0.008 and 0.046 +/- 0.017 nmol/mg Protein, respectively), and GPx activity (0.067 +/- 0.011 and 0.098 +/- 0.016 U/mg Protein, respectively).

MAIN FINDINGS: L-carnitine prevented this increase induced by diabetes; TBARS (0.039 +/- 0.006 nmol/mg Protein) and GPx activity (0.053 +/- 0.011 U/mg Protein).

CONCLUSION: These results suggest that L-carnitine exerts anti-oxidative effect in experimental diabetes....

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Journal Article 2003; 24(1-2): 86-90 PubMed PMID: 12743540 Citation  Keywords:  Animals, Antioxidants:metabolism, Glutathione Peroxidase:metabolism, Male, Malondialdehyde:metabolism, Melatonin:pharmacology, Nitric Oxide:metabolism, Rats, Rats, Wistar, Superoxide Dismutase:metabolism, Testis:drug effects, Varicocele:metabolism,.   

OBJECTIVES: The pathophysiology of the testicular damage in varicocele have not been completely understood. There are several studies concerning the effects of increased seminal reactive oxygen species (ROS) and the role of nitric oxide (NO) in infertile patients with varicocele and antioxidants have been used successfully to decrease oxidative stress in testis. In this study, we determined the effects of melatonin on testicular NO and antioxidant enzyme levels and investigated whether melatonin can prevent or diminish testicular damage in adult rats with experimentally induced unilateral varicocele.

METHODS: Thirty adult male Wistar rats were randomly divided into three groups. In group I, using midline incision left renal vein was exposed but not tied. In group II, left renal vein was partially ligated to create varicocele. In group III, after creation of varicocele, daily and fresh-prepared melatonin was administered intraperitoneally for 4 weeks. Histopathological examination was performed and tissue malondialdehyde (MDA), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and tissue NO levels were determined.

RESULTS: In group II, there were severe degenerative changes of the germinal epithelium and atrophy of the seminiferous tubules in left testis. In group III, in which rats received melatonin intraperitoneally, there were focal areas showing decrease in spermatogenesis and some degenerative changes. Similarly, the levels of ROS and NO were significantly increased in testicular tissue of rats in group II, whereas group III rat testes in which melatonin was administered, showed increased antioxidant enzyme activity and decreased NO levels.

CONCLUSION: Infertility related to varicocele has multiple pathophysiological mechanisms and the effect of ROS, NO and antioxidant defense system are contributing factors in the disease state. Melatonin, a potent free radical scavenger, administration might be helpful in the prevention or at least, in the delay of the severe effects of varicocele on testicular tissue....

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Journal Article 2001; 22(6): 417-426 PubMed PMID: 11781538 Citation  Keywords:  Aflatoxin B1:toxicity, Animals, Antioxidants:pharmacology, Apoptosis:drug effects, Caspase 3, Caspases:metabolism, Glutathione:metabolism, Glutathione Peroxidase:metabolism, Glutathione Reductase:metabolism, Glutathione Transferase:metabolism, Lipid Perox.   

OBJECTIVES: A study of liver apoptosis after aflatoxin B1 (AFB1) administration and the effect of melatonin (MEL) was investigated in male rats.

METHODS: Five groups of 15 rats each were used: controls, MEL Soln-treated rats (MEL dose,5 mg/Kg body wt), AFB1-treated rats (50 microg/Kg body wt), MEL Soln+AFB1-treated rats, and MEL micro-capsules (MEL-MC)+ AFB1-treated rats. After 8 weeks of treatment, biochemical measurements in liver homogenates and histopathological examination of liver sections of different groups using light and transmission electron microscope were done. The caspase-3 enzyme activity, apoptotic marker, was determined in liver tissues. Because hepatic antioxidants represent the major defence against toxic liver injury, and they act as anti-apoptosis. So, the levels of glutathione (GSH) and zinc (Zn) and the enzyme activities of glutathione reductase (GR), glutathione peroxidase (GSPx) and glutathione-S-transferase (GST) were determined. In addition, the levels of malondialdehyde (MDA), a lipid peroxidation product, and nitric oxide (NO) levels were measured.

RESULTS: The levels of caspase-3 activities in AFB1 group were significantly higher than control group. The apoptosis was associated with degenerative and necrotic changes in the hepatocytes. Concomitantly, the levels of MDA and NO in liver tissues were significantly increased while the levels of GSH, Zn and enzyme activities of GSPx and GR in liver tissues were significantly decreased in AFB1 group compared to their levels in controls. Caspase-3 activity was positively correlated with MDA while negatively correlated with GSH, GSPx and GR in rat livers treated with AFB1. The apoptotic rate was significantly reduced when MEL co-administrated with AFB1. In rats which received MEL with AFB1, the levels of MDA and NO in liver tissues were significantly reduced while GSH and Zn levels and GSPx, GR and GST activities were significantly increased compared to AFB1 group. When MEL-MC co-administrated with AFB1 appeared more effective in reduction of apoptotic rate as detected by decline of caspase-3 activities (inhibition 66.82%) and confirmed by histopathology.

CONCLUSION: AFB1 can lead to direct or indirect caspase-3 activation and consequently to apoptosis in rat liver. MEL treatment of rats could enhance hepatic antioxidant/detoxification system which consequently reduce the apoptotic rate and the necrobiotic changes in the liver. MEL-MC exhibited an efficient protective effect against AFB1. Thus, clinical application of MEL as therapy should be considered in cases of aflatoxicosis....

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