ascorbic-acid and erdosteine

To compare the protective efficacy of erdosteine and vitamins C and E against renal injury caused by hind limb ischemia-reperfusion (I/R).. Rats were split into 4 groups: group I as the control, group II as I/R, group III as I/R + erdosteine, and group IV as I/R + vitamins C and E. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) tissue levels were determined.. MDA levels were found comparable with the control group in groups II and III. However, they were considerably decreased in group IV when compared to group II (P < 0.01). Additionally, SOD, CAT, and GSH-Px activities were considerably (P < 0.05) decreased in group II. While CAT and GSH-Px activities were restored (P <0.01) by vitamin E and C treatment, SOD activity was not significantly affected. While GSH-Px activities were higher (P < 0.05) with erdosteine administration, SOD and CAT activities were unchanged.. The protective effect of vitamins C and E is higher than that of erdosteine treatment in reducing the oxidative stress after renal ischemia in this animal model.

Topics: Animals; Antioxidants; Ascorbic Acid; Hindlimb; Kidney; Kidney Diseases; Lipid Peroxidation; Male; Oxidoreductases; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Thioglycolates; Thiophenes; Vitamin E

The aim of this study was to investigate the protective effects of erdosteine and vitamins C and E (VCE) on the lungs after performing hind limb ischemia-reperfusion (I/R) by assessing oxidative stress, plasma copper (Cu), and zinc (Zn) analysis. The animals were divided randomly into four groups as nine rats each as follows: control, I/R, I/R plus erdosteine, and I/R plus VCE combination. I/R period for 60 min was performed on the both hind limbs of all the rats in the groups of I/R, erdosteine with I/R, VCE with I/R allowing 120 min of reperfusion. The animals received orally erdosteine one time in a day and 3 days before I/R in the erdosteine group. In the VCE group, the animals VCE combination received one time in a day and 3 days before I/R, although placebo was given to control and I/R group animals. Lung lipid peroxidation (malondialdehyde [MDA]) level, superoxide dismutase (SOD), and catalase activities were increased, although lung glutathione (GSH) and plasma Zn levels decreased in I/R group in lung tissue compared with the control group. Serum MDA level, creatine kinase, and lactate dehydrogenase activities were increased in I/R group compared with the control. Lung MDA and plasma Zn levels and lung SOD activity were decreased by erdosteine administration, whereas lung GSH levels after I/R increased. The plasma Zn levels and lung SOD activity were decreased by VCE administration, although the plasma Cu and lung GSH levels increased after I/R. In conclusion, erdosteine has an antioxidant role on the values in the rat model, and it has more protective affect than in VCE in attenuating I/R-induced lung injury in rats.

Topics: Animals; Antioxidants; Ascorbic Acid; Copper; Creatine Kinase; Expectorants; Glutathione; L-Lactate Dehydrogenase; Lower Extremity; Lung; Male; Malondialdehyde; Oxidative Stress; Protective Agents; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Thioglycolates; Thiophenes; Vitamin E; Zinc

Direct exposure in vitro of the protein alpha 1-antitrypsin (alpha 1-AT; human neutrophil elastase inhibitor, alpha 1-proteinase inhibitor) to gas phase cigarette smoke causes a loss of elastase-inhibitory capacity (EIC). This effect appears to be related to the formation of reactive oxygen species in the smoke that inactivate alpha 1-AT by oxidizing the methionine terminal amino acid. Reducing agents such as glutathione and ascorbic acid prevent this inactivation. In the present investigation erdosteine, a novel thiol derivative, which contains two blocked SH groups with potential reducing properties, was tested in vitro for its capacity to protect human alpha 1-AT. For the purpose, the compound, previously hydrolyzed with bicarbonate-carbonate buffer or with microsomal enzymes was put in contact with alpha 1-AT and exposed to gas phase cigarette smoke. The EIC of alpha 1-AT was then measured by incubating the samples with leukocyte elastase and, subsequently, by titrating the residual elastolytic activity against a synthetic substrate. Under these conditions erdosteine effectively protected alpha 1-AT against the smoke injury and, after alkaline hydrolysis, it appeared to be as active as glutathione and ascorbic acid (EC50 being respectively 6.4, 7.2 and 6.2 mM). This evidence suggests that the erdosteine SH groups, which can become free, may have an important role in the mechanism of action, by blocking highly reactive oxygen-free radicals. Erdosteine may have a therapeutic application in preventing oxidative lung damage induced by cigarette smoke.

Topics: alpha 1-Antitrypsin; Ascorbic Acid; Free Radicals; Glutathione; Humans; In Vitro Techniques; Nicotiana; Plants, Toxic; Smoke; Thioglycolates; Thiophenes