We believe that both testicular torsion and detorsion result in testicular tissue damage by means of lipid peroxidation, which is evident by an increase in the tissue levels of MDA. Dietary supplementation with GE seems to attenuate the generation of toxic free radicals, as evidenced indirectly by low tissue MDA levels.

Propofol, which is widely used as an intravenous anesthetic, has been shown to have an antioxidant activity on several tissues. This study was designed to investigate the prevention of reperfusion injury with propofol after testicular torsion. Five groups of rats (seven in each group) were used. Animals in the control group (group I) did not received any treatment, while animals in the sham group (group II) underwent scrotal incision and testicular fixation only. After 2 h of 720 degrees left testicular torsion in groups III, IV and V, subsequent detorsion was done for 2 h in groups IV and V. Propofol (50 mg/kg) was injected transperitoneally 30 min prior to detorsion in group V. Both testicles in all rats were retrieved and tissue malondialdeyhde (MDA) level, which is a measure of the amount of free oxygen radicals, and enzymatic activity of xanthine oxidase (XO), which converts hypoxanthine to xanthine and uric acid were studied. In addition, tissue catalase (CAT) and glutathione peroxidase (GSH-Px) activities, which are endogenous scavenger enzymes, protecting tissues against free radicals, were studied. Additionally, histological evaluations were performed after hematoxylin and eosin staining. Testicular MDA levels, and XO and CAT activities were higher in the torsion group compared to sham control group (P<0.05). Detorsion caused a further increase in MDA levels, contrasting with a decrease in the levels of XO activity, while CAT activity was not changed. Pretreatment with propofol prevented a further increase in MDA levels and significantly decreased CAT activity following detorsion. GSH-Px activities were not effected either by torsion/detorsion or propofol pretreatment. Histologically, torsion caused some separation between germinal cells in the seminiferous tubules, which became much more prominent in the detorsion group and attenuated with propofol pretreatment. There was no significant change in any of the above-mentioned enzymatic activities nor were there histopathological changes in the contralateral testicle in any groups. It is concluded that biochemically and histologically reperfusion injury occurs in the ipsilateral testis following detorsion up to 2 h. Preference of propofol for anaesthesia during the detorsion procedure may attenuate such reperfusion injury.

In the present study, we investigated the effects of simvastatin, a 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitor, on lipid metabolism, lipid peroxidation, antioxidant enzyme activities and ultrastructure of diabetic rat lung. Diabetes was induced by a single injection of streptozotocin (45 mg kg(-1), i.p.). After 8 weeks induction of diabetes, some control and diabetic rats were treated with simvastatin (10 mg kg(-1) rat day(-1); orally) for 4 weeks. Diabetes resulted in significantly high levels of blood glucose and plasma lipids. Malondialdehyde levels were unchanged after 12-week-old diabetic rats, whereas catalase activity significantly decreased in the lung. Glutathione peroxidase activity and nitric oxide level were significantly elevated in the diabetic lung. Histological analysis of the diabetic lung revealed some deterioration in the structure. Simvastatin treatment reduced plasma lipid levels and partially decreased the severity of hyperglycaemia. Catalase, glutathione peroxidase activities and nitric oxide levels were partially restored and accompanied by improved structure in diabetic lung by the simvastatin treatment. These results suggest that structural disturbances and alteration of antioxidative enzyme activities occurred in diabetic lung. Simvastatin treatment may provide some benefits in the maintenance of antioxidant status and structural organization of diabetes-induced injury of lung.

Our results demonstrate that cholesterol supplementation leads to dense plaque formation in the aortas of the rabbits. Garlic extract supplementation ameliorates blood lipid profile and, increases antioxidant potential. Extract treatment can significantly reduce plaque surface area in the aorta. Our results suggest that increased blood antioxidant potential due to extract supplementation might be one of the factors leading to this end.

Our results demonstrate that cholesterol supplementation leads to dense plaque formation in the aortas of the rabbits. Garlic extract supplementation ameliorates blood lipid profile and, increases antioxidant potential. Extract treatment can significantly reduce plaque surface area in the aorta. Our results suggest that increased blood antioxidant potential due to extract supplementation might be one of the factors leading to this end.

The nephrotoxic actions of aluminium (Al) arise from its accumulation in the kidneys, with the resultant degeneration of the renal tubular cells. It has been suggested that Al generates reactive oxygen species that cause the oxidative deterioration of cellular lipids, proteins, and DNA. To test this hypothesis, we have here investigated the potential for a protective role of alpha-tocopherol (vitamin E) during short-term exposure of rats to Al. Al was administered intraperitoneally either alone or in combination with vitamin E at a different point of abdomen, and the alterations in the kidney tissue were analyzed histologically. The results reveal that significant light microscopical and ultrastructural damage is caused by Al, whereas with the immediate coadministration of vitamin E, there is a protective effect against this damage to the kidney tissue. In Al-alone group, the glomeruli and proximal tubuli and the Bowman capsules had swellings, adherence, hemorrhage, increase in mesangial matrix, and marked interstitial tissue fibrosis, indicating severe damage. In the Al and vitamin E immediate coinjected group, renal tubule cells were almost of a normal appearance. A slight stenosis was seen in the capsular area in the Malpighi corpuscules. The tubular organization and the cytoplasmic basophilia were also much the same as in the control group, with the lumen clearly visible in most of the cortical tubuli. The results highlight the need to reduce exposure to Al, with particular attention being paid to the known sources of Al. At the same time, the maintenance of a diet that is rich in vitamin E should be beneficial in the alleviation of Al toxicity.

Exposure to tobacco smoke can cause irritation of the conjunctiva. We conducted this study to identify the effect of tobacco on rat conjunctiva. Animals were divided into experimental and control groups and we exposed the experimental group to tobacco smoke. Control group rats inhaled only room air. Spectrophotometric analysis of the smoke-air mixture revealed that many toxic substances were present in this compound. We found very high levels of plasma thiocyanate after exposure to smoke in experimental group animals but no increase in the control group. So, this data indicates that these animals inhaled smoke effectively in our method. After 3 months conjunctivas were examined by light and electron microscopy. In the experimental group, conjunctivas were thinned, atrophied and microvillous projections and desmosomal connections were absent in comparison with the control conjunctivas. This pathologic change is very similar to conjunctival response to chronic irritants of any type.

BackgroundDoxorubicin (brand name: Adriamycin®) is used to treat solid tissue cancer but it also affects noncancerous tissues. Its mechanism of cytotoxicity is probably related to increased oxidation, mitochondrial dysfunction, and apoptosis. Melatonin is reported to have antiapoptotic and antioxidative effects. The aim of this study was to determine whether melatonin would counteract in vitro cytotoxicity of doxorubicin in mouse fibroblasts and determine the pathway of its action against doxorubicin-induced apoptosis.Material/MethodsWe measured markers of apoptosis (cytochrome-c, mitochondrial membrane potential, and apoptotic cell number) and oxidative stress (total oxidant and antioxidant status) and calculated oxidant stress index in 4 groups of fibroblasts: controls, melatonin-treated, doxorubicin-treated, and fibroblasts concomittantly treated with a combination of melatonin and doxorubicin.ResultsMelatonin given with doxorubicin succesfully countered apoptosis generated by doxorubicin alone, which points to its potential as a protective agent against cell death in doxorubicin chemotherapy. This also implies that patients should be receiving doxorubicin treatment when their physiological level of melatonin is at its highest, which is early in the morning.ConclusionsThis physiological level may not be high enough to overcome doxorubicin-induced oxidative stress, but adjuvant melatonin treatment may improve quality of life. Further research is needed to verify our findings.