Oxidative stress in the brain of nicotine-induced toxicity: protective role ofAndrographis paniculataNees and vitamin E

Abstract

Mitochondria are the crossroads of several crucial cellular activities; they produce considerable quantities of superoxide radical and hydrogen peroxide, which can damage important macromolecules. Nicotine affects a variety of cellular processes, from induction of gene expression to modulation of enzymatic activities. The aim of this study was to elucidate the protective effects of andrographolide (ANDRO) aqueous extract (AE-Ap) of Andrographis paniculata, and vitamin E on nicotine-induced brain mitochondria. In this investigation, nicotine (1 mg.kg body mass-1.day-1) was treated, for the period of 7 days, simultaneously with 2 A. paniculata products, ANDRO and AE-Ap (250 mg.kg body mass-1.day-1); and vitamin E (50 mg.kg body mass-1.day-1) was supplemented in different group of male Wistar rats. The activities of mitochondrial electron transport chain (Mito-ETC) complexes (I, II, III), nitric oxide production, superoxide anion, catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, and concentrations of reduced glutathione and oxidized glutathione were measured in discrete regions of brain (the cerebral hemisphere, cerebellum, diencephalons, and brain stem). The study revealed that nicotine inhibits the Mito-ETC complexes and produces nitric oxide, which suppressed the mitochondrial oxidative stress scavenger system in different brain regions. In these circumstances, lipid peroxidation and protein oxidation were noted in different discrete regions of brain mitochondria. ANDRO, AE-Ap, and vitamin E showed the protective potentiality against nicotine toxicity. The analysis of such alterations is important in determining the basis of normal dysfunction in the brain associated with nicotine toxicity, which could be ameliorated by A. paniculata and vitamin E, and may help to develop therapeutic means against nicotine-induced disorders.

Brain oxidative damage restored by Sesbania grandiflora in cigarette smoke-exposed rats

“…This result was consistent with previous studies depicting that protein oxidation was elevated in cigarette smoke exposure Das et al 2009;Fraga et al 2011;Ozkol et al 2012). It was already showed that cigarette smoke causes increased generation of free radicals, mainly ROS, through the induction of various ROSproducing endogenous enzymes (Deliconstantinos and Villiotou 2000;Czekaj et al 2005;Das et al 2009;Khanna et al 2013;Jaques et al 2013). In agreement with their reports, the present results illustrated that Cyt P450, NADPH oxidase, and XO activities were increased in the brain of rats exposed to cigarette smoke.…”

Ascorbic Acid Ameliorates Nicotine Exposure Induced Impaired Spatial Memory Performances in Rats

“…It is well known that nicotine contributes a major proportion of the net oxidative stress imposed by tobacco use. Nicotine induced oxidative stress in rat brain tissue has also been reported (18). Additionally, nicotine exposure significantly increased lipid peroxidation in various tissues of rats (19).…”

“…Nicotine has been shown to produce nitric oxide, which suppresses the mitochondrial oxidative stress scavenger system in different brain regions (18). Antioxidant effects of vitamin E and C have been reported against prenatal nicotine induced oxidative stress effects in rats and in monkeys (18,22).…”

Phytochemical Extraction and Characterization of the Leaves of Andrographis Paniculata for Its Anti-Bacterial, Anti-Oxidant, Anti-Pyretic and Anti-Diabetic Activity

“…In vitro studies have shown that alloxan is selectively toxic to pancreatic beta cells, leading to the induction of cell necrosis (6) . The cytotoxic action of alloxan is mediated by reactive oxygen species, with a simultaneous massive increase in cytosolic calcium concentration, leading to rapid destruction of beta cells (12) .…”