Naltrexone Reverses Ethanol-Induced Rat Hippocampal and Serum Oxidative Damage

Abstract

Naltrexone, an antagonist of μ-opioid receptors, is clinically used as adjuvant therapy of alcohol dishabituation. The aim of the present work was to test the effect of 1 mg/kg body weight of naltrexone to revert oxidative stress-related biochemical alterations, in the hippocampus and serum of chronic alcoholic adult rats. Malondialdehyde concentration was increased and glutathione peroxidase activity was decreased in hippocampus and serum of alcohol-treated rats. Naltrexone treatment restored these alterations. The in vitro antioxidant ability of Ntx could not justify these effects considering the doses used. Thus this apparent protective effect of Ntx can only be attributed to its pharmacological effects, as herein discussed.

Effects of Acute Ethanol Administration on Brain Oxidative Status: The Role of Acetaldehyde

“…A). However, some authors have described an increase in MDA concentrations after long‐term EtOH administration, thus confirming failure of the compensatory mechanism in response to the oxidative threat after chronic exposure to alcohol (Almansa et al., ; Barcia et al., ; Johnsen‐Soriano et al., ). It is also remarkable that DP had no effect on lipid peroxidation or oxidative damage to proteins.…”

“…Previous studies have explored the effects of EtOH administration on ROS production (Guerri and Grisolia, ). In this respect, it has been described that chronic EtOH administration produces a decrease in antioxidant levels (Almansa et al., , ; Barcia et al., ; Sancho‐Tello et al., ). Moreover, treatment with antioxidants has been demonstrated to prevent functional impairments such as survival of newly formed neurons (Herrera et al., ) or alterations in long‐term potentiation induction (Johnsen‐Soriano et al., ).…”

“…In fact, chronic EtOH administration decreases the hippocampal GSH/GSSG ratio as well as GPx activity. Moreover, since ROS usually react with lipids, and the CNS is especially rich in polyunsaturated fatty acids as mentioned above, lipid peroxidation results in the production of aldehydes such as malondialdehyde (MDA; Almansa et al., ; Barcia et al., ; Hernández et al., ). Chronically, these end products may create adducts, leading to DNA and protein alterations (which can be assessed by the determination of the total carbonyl group (CG) content).…”

Does Oxidative Stress Induced by Alcohol Consumption Affect Orthodontic Treatment Outcome?

“…However, nervous tissue, diverse connective-related tissues and others are also affected. EtOH exerts its deleterious effects in several tissues via oxidative and non-oxidative metabolic pathways (Bondy and Guo, 1995) involving free radical production and lipid peroxidation (Sun et al, 1997; Bosch-Morell et al, 1998; Ramachandran et al, 2003; Almansa et al, 2013; Flores-Bellver et al, 2014). One of the most important factor in this toxic process deals with the properties of EtOH to promote reactive oxygen species (ROS).…”

Oxidative Stress and the Combined Use of Tetrahydrocannabinol and Alcohol: Is There a Need for Further Research?

“…There are many contributions demonstrating EtOH induction of oxidative stress in nerve cells. These include intracellular redox state changes, production of acetaldehyde, damage to mitochondria, direct effect on cell membrane caused by hydrophobic EtOH interactions, altered cytokine production, effects on antioxidant enzymes and chemicals, impairment of neurogenesis, and other pathways [33,[45][46][47][48][49]. Nonetheless, the main pathway appears to be the induction of CYP2E1 by EtOH, being an effective generator of ROS [33].…”