thiobarbituric-acid and Necrosis

To evaluate the effects of hypertonic saline solution associated to remote ischemic perconditioning in renal ischemia/reperfusion injury in rats.. Twenty five male rats (Wistar) underwent right nephrectomy and were distributed into five groups: Sham group (S); Ischemia/Reperfusion group (I/R) with 30 minutes of renal ischemia; Remote ischemic perconditioning group (Per) with three cycles of 10 minutes of I/R performed during kidney ischemia; Hypertonic saline solution group (HSS) treated with hypertonic saline solution (4ml/kg); remote ischemic perconditioning + Hypertonic saline solution group (Per+HSS) with both treatments. After reperfusion, blood samples were collected for BUN and creatinine serum levels analyzes. TBARS were evaluated in plasma and renal tissue to assess oxidative stress. Kidney histopathological examination were performed.. Per+HSS group showed a lower degree of renal dysfunction in relation to I/R group, whereas the technique of remote ischemic perconditioning isolated or associated with saline solution significantly reduced oxidative stress and histological damage.. Remote ischemic perconditioning associated or not to saline solution promoted reduction of acute renal injury induced by ischemia/reperfusion.

Topics: Animals; Blood Urea Nitrogen; Creatinine; Ischemia; Ischemic Preconditioning; Kidney; Kidney Function Tests; Male; Necrosis; Oxidative Stress; Protective Agents; Random Allocation; Rats, Wistar; Reperfusion Injury; Reproducibility of Results; Saline Solution, Hypertonic; Thiobarbiturates; Time Factors; Treatment Outcome

In the present study, the association between acetylcholine (ACh)-induced muscle necrosis and the appearance of lipid peroxidation products was investigated. Lipid peroxidation in this injury was quantified by the malondialdehyde-thiobarbituric acid complex (TBA-MDA) using HPLC. To induce muscle necrosis, rats were treated with 1.0 or 2.0 mg/kg diisopropylphosphorofluoridate (DFP), an irreversible inhibitor of AChE that induced muscle fasciculations, and were euthanized 30-120 min after the DFP treatment. DFP caused a dose-dependent increase in AChE inhibition, muscle fasciculations, TBA-MDA formation, and muscle necrosis. Reduction of glutathione (GSH) by pretreatment with buthionine sulfoximine (BSO) potentiated the DFP-induced changes in TBA-MDA and caused an increase in the number of necrotic muscle fibers. Prevention of fasciculations by pretreatment with cholinergic antagonists such as atropine and d-tubocurarine, before DFP, inhibited the increase in lipid peroxidation, and significantly attenuated the muscle fiber necrosis. Without affecting muscle fasciculations, the antioxidant U-78517F prevented the increase in lipid peroxidation and reduced the number of muscle fibers that became necrotic. It is suggested that DFP-induced AChE inhibition causes pronounced muscle hyperactivity as the initial step that triggers free radical-induced lipid peroxidation as the final common pathway to muscle injury.

Topics: 3,4-Methylenedioxyamphetamine; Acetylcholinesterase; Animals; Buthionine Sulfoximine; Cholinergic Fibers; Cholinesterase Inhibitors; Chromans; Diaphragm; Free Radical Scavengers; Free Radicals; Glutathione; Isoflurophate; Lipid Peroxidation; Male; Methionine Sulfoximine; Muscle Fibers, Skeletal; Necrosis; Piperazines; Rats; Rats, Sprague-Dawley; Thiobarbiturates; Tubocurarine

This study examined whether ischemia-reperfusion injury to skeletal muscle could be reduced by post-ischemic infusion of phosphoenolpyruvate (PEP) and adenosine triphosphate (ATP). The rectus femoris muscle of 54 rabbits was rendered ischemic for 3.5 hr. Eighteen rabbits received no further treatment. Thirty-six were infused intra-arterially at the end of ischemia, 18 with vehicle alone, and 18 with a mixture of PEP (80 mumol/kg) and ATP (2.6 mumol/kg). Six rabbits from each group were explored after 24 hr reperfusion and the muscles assessed for viability (by nitro blue tetrazolium), ATP (by luciferin-luciferase chemiluminescence), malonyldialdehyde (MDA) (thiobarbituric acid method), and water content. The remaining muscles in each group were examined histologically after either 1 hr or 4 days of reperfusion. At 24 hr the viability of the PEP/ATP infused muscles (78.9 +/- 15.4 percent) was significantly greater than that of untreated (41.4 +/- 27.3 percent) or vehicle-infused groups (34.0 +/- 32.7 percent). ATP stores were significantly higher and MDA (indicative of free radical activity) and water content significantly lower in the PEP/ATP treated group. At 24 hr and 4 days, muscles infused with PEP/ATP showed less necrosis and fewer infiltrating neutrophils than the untreated groups. Studies with isolated rabbit neutrophils showed that ATP alone significantly inhibited superoxide anion production by stimulated neutrophils. However, when combined with PEP at concentrations similar to those achieved in vivo, ATP did not significantly affect superoxide production. The findings indicate that post-ischemic infusion of PEP/ATP significantly reduces ischemia-reperfusion injury in rabbit skeletal muscle. The protective effect of PEP/ATP is more likely to be due to supplementation of intracellular ATP stores than to the inhibition of superoxide production by infiltrating neutrophils.

Topics: Adenosine Triphosphate; Animals; Body Water; Free Radicals; Indicators and Reagents; Injections, Intra-Arterial; Ischemia; Luminescent Measurements; Malondialdehyde; Muscle, Skeletal; Necrosis; Neutrophils; Nitroblue Tetrazolium; Pharmaceutical Vehicles; Phosphoenolpyruvate; Rabbits; Reperfusion Injury; Superoxides; Thiobarbiturates; Tissue Survival

To investigate molecular responses to lipid peroxidative stimuli in neoplastic cells, lipid peroxidation was induced in liver of rats bearing 3'-methyl-4-dimethylaminoazobenzene-induced hepatocellular carcinoma by injecting a high dose of carbon tetrachloride (CCl4), a strong lipoperoxidative reagent. Normal rat livers with or without CCl4 treatment served as controls. CCl4 administration markedly provoked fatty metamorphosis, visualized by oil red O staining, in normal livers while minimal fatty changes were seen in hepatocellular carcinomas, where necrosis was often observed instead. After CCl4 treatment, the thiobarbituric acid values (representing levels of lipid peroxides in the tissue) were increased two-fold in the untreated normal liver, but were unchanged in the cancer tissue. Levels of vitamin C, an acutely reactive antioxidant, measured by high-performance liquid chromatography were not influenced by the CCl4 injection in the cancer tissue whereas a significant decrease was evident in normal livers. The total fatty acid content, measured by gas chromatography, was significantly lower in the cancer tissue than in the normal liver while the ratio of polyunsaturated fatty acids (PUFAs) in total fatty acids was little changed. Resistance of hepatocellular cancer cells to fatty metamorphosis and their susceptibility to necrosis induced by free radicals may be due to the paucity of the target PUFAs in their cell membrane fraction, resulting in low levels of lipid peroxides. Peroxidation of PUFAs might act as a "shock absorber" against free radical-induced toxic cell death in normal cells.

Topics: Animals; Ascorbic Acid; Azo Compounds; Carbon Tetrachloride; Fatty Acids; Fatty Liver; Lipid Peroxidation; Liver; Liver Neoplasms, Experimental; Male; Methyldimethylaminoazobenzene; Necrosis; Rats; Thiobarbiturates