Ethanol induced hepatic mitochondrial dysfunction is attenuated by all trans retinoic acid supplementation

Nair, Saritha S.; Prathibha, P.; Rejitha, S.; Indira, M.

doi:10.1016/j.lfs.2015.05.023

Cited by 8 publications

(9 citation statements)

References 42 publications

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“…Furthermore, substantial collapse of mitochondrial membrane potential in response to ethanol stress was observed in mice liver. Our findings were partly consistent with earlier studies [ 5 , 26 ]. Most importantly, we further found that ethanol-induced mitochondrial damage and dysfunction were intimately related to the remodeling of mitochondrial membrane phospholipids with an enhanced amount of C18:1 and decreased content of C16:0.…”

Section: Discussionsupporting

confidence: 94%

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Zhang

et al. 2016

Nutrients

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Emerging evidence suggested mitophagy activation mitigates ethanol-induced liver injury. However, the effect of ethanol on mitophagy is inconsistent. Importantly, the understanding of mitophagy status after chronic ethanol consumption is limited. This study evaluated the effect of quercetin, a naturally-occurring flavonoid, on chronic ethanol-induced mitochondrial damage focused on mitophagy. An ethanol regime to mice for 15 weeks (accounting for 30% of total calories) led to significant mitochondrial damage as evidenced by changes of the mitochondrial ultrastructure, loss of mitochondrial membrane potential and remodeling of membrane lipid composition, which was greatly attenuated by quercetin (100 mg/kg.bw). Moreover, quercetin blocked chronic ethanol-induced mitophagy suppression as denoted by mitophagosomes-lysosome fusion and mitophagy-related regulator elements, including LC3II, Parkin, p62 and voltage-dependent anion channel 1 (VDAC1), paralleling with increased FoxO3a nuclear translocation. AMP-activated protein kinase (AMPK) and extracellular signal regulated kinase 2 (ERK2), instead of AKT and Sirtuin 1, were involved in quercetin-mediated mitophagy activation. Quercetin alleviated ethanol-elicited mitochondrial damage through enhancing mitophagy, highlighting a promising preventive strategy for alcoholic liver disease.

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Section: Discussionsupporting

confidence: 94%

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Zhang

et al. 2016

Nutrients

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“…The involvement of mitochondrial dysfunction following exposure to either acute or chronic ethanol has been well-characterized and suggested to be one of main mechanisms by which ethanol induces its injurious effects with elevated oxidative stress-mediated events and inflammation. It has been shown that many anti-oxidant substances exhibited their protective effects against ethanol-induced tissue injury by preventing mitochondrial dysfunction [67, 71]. Mitochondrial impairment has been attributed largely to increased mitochondrial oxidative stress that might result from alteration on the mitochondrial ETC via decreased levels of mitochondrial complexes, alteration of their activities, mitochondrial DNA damage, and inhibition of mitochondrial antioxidant enzymes ALDH2, glutathione peroxidase, etc [67, 71].…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that many anti-oxidant substances exhibited their protective effects against ethanol-induced tissue injury by preventing mitochondrial dysfunction [67, 71]. Mitochondrial impairment has been attributed largely to increased mitochondrial oxidative stress that might result from alteration on the mitochondrial ETC via decreased levels of mitochondrial complexes, alteration of their activities, mitochondrial DNA damage, and inhibition of mitochondrial antioxidant enzymes ALDH2, glutathione peroxidase, etc [67, 71]. This notion is in accordance with our current results where significantly altered amounts and activities of the mitochondrial ETC I, II, and III, in addition to the inactivated mitochondrial ALDH2 and decreased GSH levels were observed in ethanol-exposed mice compared to other groups.…”

Section: Discussionmentioning

confidence: 99%

Preventive effects of indole-3-carbinol against alcohol-induced liver injury in mice via antioxidant, anti-inflammatory, and anti-apoptotic mechanisms: Role of gut-liver-adipose tissue axis

Choi

Abdelmegeed

Song

2018

The Journal of Nutritional Biochemistry

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Indole-3-carbinol (I3C), found in Brassica family vegetables, exhibits antioxidant, anti-inflammatory, and anti-cancerous properties. Here, we aimed to evaluate the preventive effects of I3C against ethanol (EtOH)-induced liver injury and study the protective mechanism(s) by using the well-established chronic-plus-binge alcohol exposure model. The preventive effects of I3C were evaluated by conducting various histological, biochemical, and real-time PCR analyses in mouse liver, adipose tissue, and colon, since functional alterations of adipose tissue and intestine can also participate in promoting EtOH-induced liver damage. Daily treatment with I3C alleviated EtOH-induced liver injury and hepatocyte apoptosis, but not steatosis, by attenuating elevated oxidative stress, as evidenced by the decreased levels of hepatic lipid peroxidation, hydrogen peroxide, CYP2E1, NADPH-oxidase, and protein acetylation with maintenance of mitochondrial complex I, II, and III protein levels and activities. I3C also restored the hepatic antioxidant capacity by preventing EtOH-induced suppression of glutathione contents and mitochondrial aldehyde dehydrogenase-2 activity. I3C preventive effects were also achieved by attenuating the increased levels of hepatic proinflammatory cytokines, including IL1β, and neutrophil infiltration. I3C also attenuated EtOH-induced gut leakiness with decreased serum endotoxin levels through preventing EtOH-induced oxidative stress, apoptosis of enterocytes, and alteration of tight junction protein claudin-1. Furthermore, I3C alleviated adipose tissue inflammation and decreased free fatty acid release. Collectively, I3C prevented EtOH-induced liver injury via attenuating the damaging effect of ethanol on the gut-liver-adipose tissue axis. Therefore, I3C may also have a high potential for translational research in treating or preventing other types of hepatic injury associated with oxidative stress and inflammation.

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“…Individuals with chronic AUD are generally malnourished (Chopra and Tiwari, 2012;Clugston and Blaner, 2012;Nair et al, 2015;Ross et al, 2012). Alcohol both inhibits the absorption of many nutrients directly (Badawy, 2014) and, with chronic alcohol intake, can also severely impact the health of the entire gastrointestinal (GI) tract.…”

Section: Nutritional Intake and Absorptionmentioning

confidence: 99%

The importance of nutrition in aiding recovery from substance use disorders: A review

Jeynes

Gibson

2017

Drug and Alcohol Dependence

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Ethanol induced hepatic mitochondrial dysfunction is attenuated by all trans retinoic acid supplementation

Cited by 8 publications

References 42 publications

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Preventive effects of indole-3-carbinol against alcohol-induced liver injury in mice via antioxidant, anti-inflammatory, and anti-apoptotic mechanisms: Role of gut-liver-adipose tissue axis

The importance of nutrition in aiding recovery from substance use disorders: A review

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