Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure

Abstract

Both aluminum and ethanol are pro-oxidants and neurotoxic. Considering the possibilities of co-exposure and sharing mechanisms of producing neurotoxicity, the present study was planned to identify the level of aluminum-induced oxidative stress in altered pro-oxidant (ethanol exposure) status of cerebrum. Male rats were coexposed to aluminum and ethanol for 4 weeks. After the exposure period, cerebral levels of protein, reduced glutathione (GSH), lipid peroxidation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) of cerebrum were estimated. In most of the cases significant correlations were observed between the alterations and graded ethanol doses, suggesting a dose-dependency in pushing the oxidant equilibrium toward pro-oxidants. Aluminum is found to influence significantly all the studied parameters of oxidative stress. Likewise, ethanol also influenced these parameters significantly, except GR, while the interaction between ethanol and aluminum could significantly influence only the GSH content and GR activity of cerebrum. Present study demonstrate that coexposure of aluminum with pro-oxidant might favor development of aluminum-induced oxidative stress in cerebrum. This observation might be helpful in understanding of mechanism of neurodegenerative disorders and ameliorate them.

Evaluation of the protective effect of Prunus amagdylus against aluminium chloride induced neurochemical alterations and spatial memory deficits in rats

“…AlCl3 is a non-redox active metal capable of increasing the cellular oxidative milieu by potentiating the pro-oxidant properties. 37 Chronic AlCl3 exposure generates reactive oxygen species (ROS) that cause lipid peroxidation (LPO) and oxidative damage to proteins, DNA, and decreasing intracellular antioxidants. Our results strongly support the hypothesis that the memory deficits observed after chronic alumin iu m chloride treatment might have arisen as a result of ROS mediated mitochondrial dysfunction, ultimately causing oxidative injury to neurons, resulting in evident neuroinflammation which could therefore, be prevented by antioxidant treatment.…”

Interplay of glia activation and oxidative stress formation in fluoride and aluminium exposure

“…The induction of oxidative stress strongly correlates with the activation of glial astrocytic cells, microglial cells and B-cells. Although the exact mechanism of fluoride and aluminium toxicity still remains largely unknown, these substances have been reported to generate high levels of free radicals when either given alone or in combination [23][24][25][26][27]. The redox balance of cells maintained by oxidants and antioxidants are important to physiological activities and functions [23].…”

“…Hence, disturbance of the natural equilibrium by increased generation of free radicals causes cellular dysfunctions and promotes oxidative damages to tissues [23]. Fluoride and aluminium have been reported to affect cellular enzymes, especially antioxidants by inducing oxidative stress [24][25][26][27]. Oxidative stress is caused by the production of reactive oxygen species (ROS).…”

“…SOD is a metallo-protein that facilitates the elimination of the primary toxicity of superoxide and the secondary toxicity of hydroxide and hydrogen peroxide by decreasing the concentrations of superoxide [26]. Their conversion into less harmful products is of critical importance for living cells.…”

Pro-oxidant status based alterations in cerebellar antioxidant response to aluminum insult

“…Oteiza et al [5] have demonstrated that alumi num can behave as both pro oxidant and antioxidant depending on its concentration, presence of Fe 2+ and integrity of the membrane. Recently, compromization of antioxidative responses in cerebrum has been dem onstrated by the presence of aluminum [6] and it has 1 The article is published in the original. 2 been suggested that though direct role of aluminum as oxidative stressor is questionable, nonetheless, it can elevate the oxidative stress if brain is already facing some oxidant insults [4,6].…”