Omer Coskun

Vitamin E against oxidative damage caused by formaldehyde in frontal cortex and hippocampus: biochemical and histological studies.

Formaldehyde (FA) can cause severe central nervous system impairment. But, there are only a few studies about biochemical and histopathological changes of frontal cortex and hippocampal tissue caused by FA toxicity. The aim of our study was to investigate these changes occurring after chronic formaldehyde toxicity in frontal cortex and hippocampal tissues, and protective effect of Vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control, (2) treated with FA (FAt), and (3) treated with FA and vit E (FAt+vit E) groups. After the treatment, the animals were sacrificed and frontal cortex and hippocampal tissues were removed for biochemical and histopathological investigation. FA significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in frontal cortex and hippocampal tissue compared to control. Vit E treatment decreased MDA and PC levels and prevented inhibition of SOD and CAT enzymes in the tissues. In the FAt group, the neurons of both tissues became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in FAt+vit E group was protected well, but not as neurons of the control group. The number of neurons in frontal cortex and hippocampal tissue of FAt group was significantly less than both control and FAt+vit E groups. It was concluded that vit E treatment might be beneficial in preventing FA-induced oxidative frontal cortex and hippocampal tissue damage, therefore, shows potential for clinical use.

Contribution of flavonoid antioxidants to the preventive effect of mesna in cyclophosphamide-induced cystitis in rats.

Cyclophosphamide (CP) is widely used, alone or in combination with other chemotherapeutic agents, for treatment of neoplastic diseases. Its urotoxicity may cause dose-limiting side-effects, for example hemorrhagic cystitis. The agent most often used to prevent this side-effect is mesna (2-mercaptoethane sulfonate). Overproduction of reactive oxygen species during inflammation is one reason for possible urothelial injury. The aim of this study was to evaluate whether combinations of quercetin and epigallocatechin 3-gallate (EGCG), flavonoid antioxidants and mesna could prevent cystitis induced by cyclophosphamide, better than mesna alone. A total of 38 male Sprague–Dawley rats were divided into five groups. Four groups received single dose of CP (100xa0mgxa0kg−1) intraperitoneally at the same time. Group 2 received CP only, group 3 received mesna (3×21.5xa0mgxa0kg−1), group 4 received a single dose of mesna+EGCG (2×20xa0mgxa0kg−1), and group 5 received a single dose of mesna+quercetin (2×20xa0mgxa0kg−1), before and after CP injection. Group 1 (not treated) served as control. CP injection alone resulted in severe cystitis. Mesna resulted in some, but not full, protection against CP toxicity. Quercetin and catechine, together with mesna, resulted in full protection against CP toxicity, on the basis of histopathology of the urinary bladder. It was concluded that oxidants might be important in the pathogenesis of CP-induced cystitis, and that flavonoid antioxidants, used in addition to mesna, may help to ameliorate bladder damage.

Beneficial effects of melatonin on reperfusion injury in rat sciatic nerve.

Abstract:u2002 Studies have shown that ischemia–reperfusion (I/R) produces free radicals leading to lipid peroxidation and to damage of the nervous tissue. Melatonin, a main secretory product of the pineal gland, has free radical scavenging and antioxidant properties and has been shown to diminish I/R injury in many tissues. There are a limited number of studies related to the effects of melatonin on I/R injury in the peripheral nervous system. Therefore, in the present study, the protective effect of melatonin was investigated in rats subjected to 2u2003hr of sciatic nerve ischemia followed by 3u2003hr of reperfusion. Following reperfusion, nerve tissue samples were collected for quantitative assesment of malondialdehyde (MDA), an oxidative stress marker, and superoxide dismutase (SOD), a principal antioxidant enzyme. Samples were further evaluated at electron microscopic level to examine the neuropathological changes. I/R elevated the concentration of MDA significantly while there was a reduction at SOD levels. Melatonin treatment reversed the I/R‐induced increase and decrease in MDA and SOD levels, respectively. Furthermore, melatonin salvaged the nerve fibers from ischemic degeneration. Histopathologic findings in the samples of melatonin‐treated animals indicated less edema and less damage to the myelin sheaths and axons than those observed in the control samples. Our results suggest that administration of melatonin protects the sciatic nerve from I/R injury, which may be attributed to its antioxidant property.

The Effect of Hyperbaric Oxygen Treatment on the Renal Functions in Septic Rats: Relation to Oxidative Damage

PurposeTo investigate the effects of hyperbaric oxygen (HBO) treatment on renal functions and damage in septic rats.MethodsThe animals were divided into four groups, each containing ten animals: control, hyperbaric oxygen, sepsis, and sepsis/hyperbaric oxygen. One milliliter of saline containing live Escherichia coli cells (2.1 × 109) was injected intraperitoneally to induce sepsis. The groups treated with HBO were given five sessions of 2 atmospheres absolute of 100% oxygen at intervals of 6u2009h. Blood, urine, and tissue samples were then collected, and the functional renal parameters, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and catalase activities were examined.ResultsThe reduced glomerular filtration rate and urine flow returned to normal levels after HBO treatment; however, the increase in fractionated sodium excretion continued. The increased MDA levels in the renal cortex and medulla also decreased to the level of the control group. In the sepsis group, both the SOD and catalase activities decreased in the renal cortex, while a reduction was observed only in the catalase activity in the medulla. The reduced enzyme activities significantly increased in the sepsis/hyperbaric oxygen group.ConclusionHBO treatment has a beneficial effect on renal dysfunction in sepsis. The probable reason for this effect is the reduction in oxidative damage because of the increase in antioxidative capacity.

The oxidative and morphological effects of high concentration chronic toluene exposure on rat sciatic nerves.

This study was designed to investigate the effects of chronic toluene inhalation in high concentration on lipid peroxidation, antioxidant enzyme activities and ultrastructural changes in the sciatic nerves of rats. Male Wistar albino rats (150–250 g) were divided in two experimental groups: the control and the toluene treated group (n=10 for each). Toluene treatment was performed by inhalation of 3000 ppm toluene, in a 8 h/day and 6 day/week order for 16 weeks. Blood and tissue samples were obtained for biochemical and histopathological investigation. The blood and sciatic nerves were assayed for toluene by gas chromatography. Toluene significantly increased blood and tissue malondialdehyde (MDA), and decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but not tissue catalase (CAT) levels when compared with controls. Electron micrographs of sciatic nerve in the toluene group shows myelin destructions with onion-bulb and bubble form protrusion on the myelin sheath and axolemma border of myelinated axons. The area of injury on the myelin sheath were measured by Image-Pro Plus. Mean of the injury area were estimated 34% each myelin. These findings indicate that chronic toluene inhalation might be involved with free radical processes.