Effects of moderate alcohol consumption on oxidative stress

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Effects of moderate alcohol consumption on oxidative stress

Received Jun 15; Accepted Sep This article has been cited by other articles in PMC. Importantly, chronic alcohol use is reported to exacerbate HIV pathogenesis.

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Although alcohol is known to increase oxidative stress, especially in the liver, there is no clinical evidence that alcohol increases oxidative stress in HIV positive patients.

The mechanism by which alcohol increases oxidative stress in HIV positive patients is also unknown. Strict inclusion and exclusion criteria were applied to reduce the effect of other therapeutic drugs metabolized via the hepatic system as well as the effect of co-morbidities such as active tuberculosis on the interaction between alcohol and HIV infection, respectively.

Blood samples were collected from HIV-negative alcohol-users and HIV positive alcohol-users followed by collection of plasma and isolation and fractionation of monocytes from peripheral blood. We then determined oxidative DNA damage, glutathione level, alcohol level, transcriptional level of cytochrome P 2E1 CYP2E1 and several antioxidant enzymes, and plasma level of cytokines.

These results suggest an increase in oxidative stress in HIV-positive alcohol users compared with HIV-negative alcohol users.

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We also examined whether alcohol metabolism, perhaps by CYP2E1, and antioxidant enzymes are involved in alcohol-mediated increased oxidative stress in HIV-positive patients. The enhanced oxidative stress is accompanied by a failure of cellular antioxidant mechanisms to maintain redox homeostasis.

Alcohol, HIV, Oxidative stress, Cytochrome P, Antioxidant enzymes, Cytokines Background Chronic alcohol consumption is known to increase the incidence of acquiring HIV infection due to elevated propensity for risky sexual practices following drinking [ 1 ].

The consumption of alcohol amongst HIV patients is known to enhance HIV pathogenesis and disease progression, especially in patients who are not receiving antiretroviral therapy ART yet [ 4 — 6 ]. Moreover, studies with non-human primates have shown increased viral load upon alcohol consumption [ 7 ].

The exact mechanisms that govern the interaction between alcohol and HIV pathogenesis remains unclear. An in vitro study has suggested a possible role of oxidative stress in increasing HIV replication [ 8 ]. However, there is no clinical data on the in vivo involvement of alcohol-mediated oxidative stress in HIV replication.

Our previous studies have demonstrated the possible involvement of cytochrome P 2E1 CYP2E1 -mediated alcohol-induced oxidative stress in HIV systems including blood monocytes [ 910 ].

Effects of moderate alcohol consumption on oxidative stress

CYP2E1 is the major CYP isoform responsible for the metabolism of alcohol in chronic users, and is induced following chronic alcohol exposure [ 1112 ]. The metabolism of alcohol by CYP2E1 is known to generate reactive oxygen species ROSwhich eventually increases oxidative stress in the cells, especially those in the liver [ 13 ].

Thus, CYP2E1-mediated oxidative stress has been implicated in modulating the harmful effects of alcohol in the liver [ 14 ]. In addition to CYP2E1-mediated increased oxidative stress by alcohol, a decreased level of antioxidant enzymes AOEs may also cause an increase in alcohol-mediated oxidative stress [ 15 ].

Similarly, glutathione S-transferase kappa 1 GSTK1 is a mitochondrial antioxidant enzyme responsible for protecting mitochondrial components against oxidative stress [ 17 ].

Oxidative Stress, Prooxidants, and Antioxidants: The Interplay

In this study, we examined the effects of alcohol use in HIV positive patients through possible involvement of oxidative stress and mediators that produce oxidative stress in HIV positive alcohol users using clinical samples from well-characterized patients.

The average viral load was Alcohol, Oxidative Stress, and Free Radical Damage Defeng Wu, Ph.D., and Arthur I. Cederbaum, Ph.D. the excessive generation of molecules and oxidative stress in alcohol toxicity.

of Pharmacology and Biological Chemistry, called free radicals, Alcohol, Oxidative Stress, and Free Radical Damage. Thrive+ After-Alcohol Aid is designed specifically to mitigate the negative effects of alcohol. It works by reducing short-term alcohol withdrawal, replacing lost vitamins, and providing your liver with what it needs to break down alcohol and its toxic by-products.

Initially, 20 mg PO once daily in the morning with food. After 7 to 14 days, the dose may be increased to 40 mg PO once daily to attain target blood pressure goals; evaluate blood pressure response after 7 .

To examine the effects of alcohol use on oxidative stress we recruited HIV+ patients who reported mild-to-moderate alcohol use.

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Strict inclusion and exclusion criteria were applied to reduce the effect of other therapeutic drugs metabolized via the hepatic system as well as the effect of co-morbidities such as active tuberculosis on the interaction between alcohol and HIV infection, respectively.

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mg subcutaneously once weekly.

Effects of moderate alcohol consumption on oxidative stress

Administer the dose at any time of day, with or without meals. The dosage may be increased to mg subcutaneously once weekly if the glycemic response is inadequate.

Ethanol (Alcohol) Metabolism: Acute and Chronic Toxicities