Hydrogen peroxide affects contractile activity and anti‐oxidant enzymes in rat uterus

Abstract

Background and purpose:The effects of hydrogen peroxide (H2O2) on uterine smooth muscle are not well studied. We have investigated the effect and the mechanism of action of exogenous hydrogen peroxide on rat uteri contractile activity [spontaneous and calcium ion (Ca 2+ )-induced] and the effect of such treatment on anti-oxidative enzyme activities. Experimental approach: Uteri were isolated from virgin Wistar rats and suspended in an organ bath. Uteri were allowed to contract spontaneously or in the presence of Ca 2+ (6 mM) and treated with H2O2 (2 mM-3 mM) over 2 h. Anti-oxidative enzyme activities (manganese superoxide dismutase-MnSOD, copper-zinc superoxide dismutase-CuZnSOD, catalase-CAT, glutathione peroxidase-GSHPx and glutathione reductase-GR) in H2O2-treated uteri were compared with those in uteri immediately frozen after isolation or undergoing spontaneous or Ca 2+ -induced contractions, without treatment with H2O2. The effect of inhibitors (propranolol, methylene blue, L-NAME, tetraethylamonium, glibenclamide and 4-aminopyridine) on H2O2-mediated relaxation was explored. Key results: H2O2 caused concentration-dependent relaxation of both spontaneous and Ca 2+ -induced uterine contractions. After H2O2 treatment, GSHPx and MnSOD activities were increased, while CuZnSOD and GR (In Ca 2+ -induced rat uteri) were decreased. N w -nitro-L-arginine methyl ester antagonized the effect of H2O2 on Ca 2+ -induced contractions. H2O2-induced relaxation was not affected by propranolol, potentiated by methylene blue and antagonized by tetraethylamonium, 4-aminopyridine and glibenclamide, with the last compound being the least effective. Conclusions and implications: H2O2 induced dose-dependent relaxation of isolated rat uteri mainly via changes in voltagedependent potassium channels. Decreasing generation of reactive oxygen species by stimulation of anti-oxidative pathways may lead to new approaches to the management of dysfunctional uteri.

Down-Regulation of NFkB, Bax,TGF-β, Smad-2mRNA expression in the Livers of Carbon Tetrachloride Treated Rats using Different Natural Antioxidants

“…Cirrhosis is the end stage of both liver fibrosis and liver disease, continues one of the leading causes of death because of the increased risk for developing varietal bleeding, hepatic failure, and hepatocellular carcinoma (HCC) (D'Amico et al 2006;Rincón et al 2013). Generation of free radicals and oxidative stress plays a major role in liver toxicity induced by chemicals (Muhtaseb et al 2008, Appiah et al 2009). Carbon tetrachloride is one of the xenobiotic hazardous hepatotoxin (Xiao et al 2012), which causes liver damage through lipid peroxidation and oxidative stress (Moreria et al 2014).…”

“…It decreased the activity of Catalase (CAT), Superoxide dismutase (SOD), Glutathione-S-transferase (GST), Glutathione peroxidase (GSH-Px), Glutathione reductase (GSR), Reduced glutathione (GSH) while increased estimation of lipid peroxidation.Exposure of CCl 4 elicited the hepatic DNA damages. It was documented that natural drugs with antioxidant potential can protect the liver from damage caused by CCl 4 (Sanmugapriya and Venkataraman 2006;Appiah et al 2009;Andritoiu et al2014). CCl 4 was shown to increase the level of ALT, while it decreased the B-cell lymphoma 2 (Bcl2) level in rats (Xiao et al 2013;Mohamed et al 2015).…”

Antioxidant and hepatoprotective effects ofSolanum xanthocarpumleaf extracts against CCl4-induced liver injury in rats

“…Antioxidants are free radical scavengers (FRS) which postpone the oxidation and block the chain initiated by high energy molecules and other consequent reactions (Cespecles et al, 2008). Hepatotoxic chemicals cause liver damage which are induced by lipid peroxidation and other oxidative damage (Appiah et al, 2009). Several compounds, such as carbon tetrachloride (CC1 4 ), acetaminophen, bromobenzene, ethanol and polycyclic aromatic hydrocarbons, have been implicated in the etiology of liver diseases (Adesanoye & Farombi, 2010).…”

Piperine and Its Various Physicochemical and Biological Aspects: A Review

“…Piperine inhibit pulmonary cytochrome P450 activities [92] Piperine inhibit UDP-glucose dehydrogenase and UDP-glucuronyl transferase [98] Piperine shows antileishmanic activity [155] Piperine increases serum response of β-carotene [100] Piperine inhibit alfatoxins B1 (AFB 1 )biosynthesis [156] Piperine shows antimalarial activity [157] Piperine reduced the production of alfatoxins [158] Thermogenic action of piperine via adrenal catecholamine secretion [159] Piperine inhibit monoamine oxidase [160] Piperine inhibit ascorbate-Fe ++ -induced lipid peroxidation [161] Piperine protected against oxidative stress induced carcinogenesis [162] Piperine modulated membrane dynamics and permeation characteristics [162] Piperine shows chemopreventive effectin carcinogenesis [163,164] Piperine inhibited mitochondrial oxidative phosphorylation [165] Piperine exerted protection against t-butyl hydroperoxide [166] Piperine protects cisplatin-induced apoptosis via heme oxygenase-1 [167] Piperine potentiate hepatotoxicity of carbon tetrachloride in rats [168] Inhibition /quenching of super oxides and hydroxyl radicals by piperine [169] Piperine reduces high fat diet induced oxidative stress [170] Anti-metastatic activity of piperine on lung metastasis [171] Piperine inhibits platelet aggregation as a TXA 2 receptor antagonist [172] Piperine decreased mitochondrial lipid peroxidation [173] Piperine alleviates hypertension induced by NO synthase inhibition [174] Piperine reduced D-galactosamine induced hepatotoxicity [175] Piperine inhibited cholesteryl ester (CE) synthesis [176] Piperine enhances bioavailability of the tea polyphenol [177] Piperine shows anti mutagenic activity [178,179] Piperine shows anti-thyroid activity [180] Piperine modulates hormonal and apo lipoprotein profiles …”