Association between alcohol-induced oxidative stress and membrane properties in synaptosomes: A protective role of vitamin E

Reddy, Vaddi Damodara; Padmavathi, P.; Bulle, Saradamma; Hebbani, Ananda Vardhan; Marthadu, Shakeela Begum; Venugopalacharyulu, N.Ch; Maturu, Paramahamsa; Nallanchakravarthula, Varadacharyulu

doi:10.1016/j.ntt.2017.07.004

Cited by 25 publications

(12 citation statements)

References 30 publications

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“…Increased generation of reactive oxygen species (ROS) in the nervous tissue seems to modulate CSD susceptibility (Netto and Martins-Ferreira, 1989; El-Bachá et al, 1998; Mendes-da-Silva et al, 2014). A scenario of increased ROS production is certainly present in organisms under chronic ethanol consumption (Brocardo et al, 2017; Reddy et al, 2017). Using various paradigms of ethanol administration, we investigated the effects of ethanol on CSD propagation in the rat cortex.…”

Section: Electrophysiological Effects Of Aging: Studies Using the Sprmentioning

confidence: 99%

Brain Aging and Electrophysiological Signaling: Revisiting the Spreading Depression Model

Guedes

Abadie-Guedes

2019

Front. Aging Neurosci.

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As a consequence of worldwide improvement in health care, the aging portion of the human population has increased, now representing a higher proportion of the total population. This fact raises great concern regarding how to age while maintaining good brain function. Very often, alterations in brain electrophysiological signaling are associated with age-dependent functional disorders of the brain. Therefore, animal models suitable for the study of age-related changes in electrical activity of the brain can be very useful. Herein, we review changes in brain electrophysiological features as a function of age by analyzing studies in the rat brain on the phenomenon known as cortical spreading depression (CSD). Alterations in the brain’s capability to generate and propagate CSD may be related to differences in the propensity to develop certain neurological diseases, such as epilepsy, stroke, and migraine, which can biunivocally interact with the aging process. In this review, we revisit ours and others’ previous studies on electrophysiological features of the CSD phenomenon, such as its velocity of propagation and amplitude and duration of its slow negative DC shift, as a function of the animal age, as well as the interaction between age and other factors, such as ethanol consumption, physical exercise, and nutritional status. In addition, we discuss one relatively new feature through which CSD modulates brain signaling: the ability to potentiate the brain’s spontaneous electrical activity. We conclude that the CSD model might importantly contribute to a better understanding of the aging/brain signaling relationship.

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Section: Electrophysiological Effects Of Aging: Studies Using the Sprmentioning

confidence: 99%

Brain Aging and Electrophysiological Signaling: Revisiting the Spreading Depression Model

Guedes

Abadie-Guedes

2019

Front. Aging Neurosci.

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“…Cell membrane fluidity can be detected by fluorescence polarization, by measuring the strength of the fluorescence [13]. The increase in fluorescence polarization represented the decrease in membrane fluidity.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of the Liver Toxicity of Pterocephalus hookeri Extract via Triggering Necrosis

Wang

Dong

Zhang

et al. 2019

Toxins

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Pterocephalus hookeri (C. B. Clarke) Höeck, recorded in the Chinese Pharmacopoeia (2015 version) as a Tibetan medicine for the treatment of various diseases, especially rheumatoid arthritis, was believed to possess a slight toxicity. However, hardly any research has been carried out about it. The present study aimed to evaluate the toxicity in vivo and in vitro. Toxicity was observed by the evaluation of mice weight loss and histopathological changes in the liver. Then, the comparison research between ethyl acetate extract (EAE) and n-butanol extract (BUE) suggested that liver toxicity was mainly induced by BUE. The mechanical study suggested that BUE-induced liver toxicity was closely associated with necrosis detected by MTT and propidium iodide (PI) staining, via releasing lactate dehydrogenase (LDH), reducing the fluidity, and increasing the permeability of the cell membrane. Western blot analysis confirmed that the necrosis occurred molecularly by the up-regulation of receptor-interacting protein kinase 1 (RIP1) and receptor-interacting protein kinase 3 (RIP3), as well as the activation of the nuclear factor-kappa-gene binding (NF-κB) signaling pathway in vivo and in vitro. This finding indicated that the liver toxicity induced by BUE from P. hookeri was mainly caused by necrosis, which provides an important theoretical support for further evaluation of the safety of this folk medicine.

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“…Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamicpituitary-adrenal axis appear to be implicated in this process [92][93][94][95][96][97]. Oxidative stress also leads to the indirect damage of nerve fibers via the release of free radicals and proinflammatory cytokines with protein kinase C and ERK kinase phosphorylation [98][99][100][101]. Besides, ALN is characterized by insulin and insulin-like growth factor (IGF) resistance, which results in impaired trophic factor signaling [102,103].…”

Section: Aln Pathophysiologymentioning

confidence: 99%

Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options

et al. 2020

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Purpose of the Review Alcohol abuse causes a wide range of disorders that affect the nervous system. These include confusion, cerebellar ataxia, peripheral neuropathy, and cognitive impairment. Chronic and excessive alcohol consumption is the primary cause of peripheral neuropathy. It is worth noting that peripheral neuropathy has no reliable treatment due to the poor understanding of its pathology. Recent Findings Coasting is a major feature of alcoholic neuropathy, largely due to chronic alcohol abuse. Its major features are hyperalgesia, allodynia, and burning pain. Even though much research was done in this area, still we do not have a full understanding of the mechanism of alcoholic neuropathy. However, some theories have been proposed. These include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis also seem to be implicated in the pathophysiology of this alcoholic neuropathy. The goal of treatment is to impede further damage to the peripheral nerves while also restoring their normal physiology. Alcohol abstinence, intake of balanced diets, and treatment with medications are suggested including benfotiamine, alpha-lipoic acid, acetyl-l-carnitine, vitamin E, methylcobalamin, myo-inositol, N-acetylcysteine, capsaicin, tricyclic antidepressants, or antiepileptic drugs. Summary This review focuses on the many pathways that play a role in the onset and development of alcohol-induced neuropathy, as well as present the possible treatment strategies of this disorder, providing insights into a further search of new treatment modalities.

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Association between alcohol-induced oxidative stress and membrane properties in synaptosomes: A protective role of vitamin E

Cited by 25 publications

References 30 publications

Brain Aging and Electrophysiological Signaling: Revisiting the Spreading Depression Model

Brain Aging and Electrophysiological Signaling: Revisiting the Spreading Depression Model

Evaluation of the Liver Toxicity of Pterocephalus hookeri Extract via Triggering Necrosis

Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options

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