The effect of melatonin on lipid peroxidation during radiotherapy in female rats

Background: Because radiotherapy is one of the causes of primary or secondary ovarian failure, protection of ovarian functions in the patients receiving total body or pelvic radiotherapy is of importance. In this study, we investigated the role of melatonin in the oxidative damage in both whole body and ovaries, which is caused by radiotherapy. Materials and Methods: Eighteen female rats were divided into 3 groups, each of which consisted of 6 rats. First group was control group receiving no treatment, second group received total body radiotherapy (RT) by 2 x 360 cGy only and third group received radiotherapy plus melatonin. Malondialdehyde (MDA) levels in both blood and ovarian tissue were detected as the indicator of free radical (FR) damage. Levels of erythrocyte superoxide dismutase (SOD) and glutathion peroxidase (GPX) in blood were measured as the indicators of antioxidant level. Results: Radiotherapy caused a significant increase in the levels of MDA in blood and ovarian tissue (p < 0.001). However, MDA levels decreased in the radiotherapy plus melatonin group (p < 0.05). SOD and GPX levels decreased insignificantly in the radiotherapy only group while they increased in the radiotherapy plus melatonin group significantly (p < 0.01 and p < 0.05, respectively). Conclusion: Melatonin, in rats, reduced the level of MDA, which is elevated by radiotherapy and increased the levels of SOD and GPX, which are involved in the antioxidant system

effect of exogenous sulfite ingestion

Sulfites whether ingested or produced through the sulfur-containing amino acids metabolism of the animal are very active molecules and can cause cellular toxicity. Sulfite oxidase (SOX), a heme- and molybdenum containing mitochondrial enzyme, prevents mammalian cells from adverse effects of sulfite toxicity by metabolizing sulfite to sulfate. The present study was aimed to investigate effect of sulfite on the N-methyl-(D)-aspartate (NMDA) receptor (NMDAR) NR2A and NR2B subunits in hippocampus of normal and SOX-deficient rats. Rats were divided into four groups; (1) control group, which was given rat chow and tap water ad libitum (C), (2) sulfite group, treated with sulfite (25 mg/kg) in drinking water and commercial rat chow ad libitum (S), (3) SOX-deficient group, maintained on high-W/Mo-deficient regimen to produce SOX deficiency (D), and (4) SOX-deficient + sulfite group (DS), prepared as those in the third group and were afterwards given sulfite (25 mg/kg) additionally. Whole treatment schedule were continued for 6 weeks. Sulfite treatment caused a decrease of NR2A and NR2B subunits of the NMDAR in hippocampus of rats in S and DS groups. Interestingly, similar decrement was observed in D group, probably due to increased endogen sulfite production. In summary, the results indicated that feeding sulfite to the rats may cause down-regulation of NMDARs by degrading NR2A and NR2B subunits of it, which may be considered as a neuro-compensatory mechanism