Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice

Hu, Chunqiu; Bo, Qingli; Chu, Leung Wing; Hu, Yong-Di; Fu, Lin; Wang, Guoxiu; Lü, Yan; Liu, Xiaojing; Wang, Hua

doi:10.1155/2020/5715893

Cited by 15 publications

(10 citation statements)

References 54 publications

(58 reference statements)

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“…Furthermore, alcohol-dependent individuals often exhibit low vitamin D levels as a direct result of how alcohol exerts its influence on vitamin D metabolism (malabsorption of vitamin D, decreased levels of the vitamin-D binding protein, reduced ability to hydroxylate vitamin D in the liver), altered biliary excretion, insufficient food intake, or reduced sun exposure. Studies conducted on animals have shown that chronic alcohol use may result in decreased serum concentrations of 1,25-dihydroxyvitamin D due to impaired renal synthesis and/or increased degradation of 1,25-dihydroxyvitamin D. Further research is needed to identify different mechanisms which contribute to low vitamin D levels associated with excessive alcohol use or intoxication [ 12 , 27 , 28 , 29 ]. Chun-Qiu Hu et al (2020) conducted a study on animals and found that vitamin D deficiency exacerbates cellular apoptosis in alcohol-induced liver damage (it leads to hepatic inflammation and oxidative stress—through regulation of oxidative and antioxidant enzymes) [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

“…Studies conducted on animals have shown that chronic alcohol use may result in decreased serum concentrations of 1,25-dihydroxyvitamin D due to impaired renal synthesis and/or increased degradation of 1,25-dihydroxyvitamin D. Further research is needed to identify different mechanisms which contribute to low vitamin D levels associated with excessive alcohol use or intoxication [ 12 , 27 , 28 , 29 ]. Chun-Qiu Hu et al (2020) conducted a study on animals and found that vitamin D deficiency exacerbates cellular apoptosis in alcohol-induced liver damage (it leads to hepatic inflammation and oxidative stress—through regulation of oxidative and antioxidant enzymes) [ 29 ]. There are also studies showing that excessive alcohol use is associated with increased serum levels of 25 (OH) D [ 30 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

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Association between Vitamin D and Cognitive Deficiency in Alcohol Dependence

et al. 2022

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There are still not enough findings to elucidate how exactly alcohol use impairs cognitive abilities. Some studies have shown that there is a link between alcohol intake and vitamin D levels, but these findings are inconsistent so further research is needed. The aim of this study was to investigate the association between serum vitamin D levels and cognitive impairment in alcohol-dependent individuals. A case-control study was carried out including a total of N = 132 respondents with a medical history of alcoholism, and healthy volunteers. The Montreal Cognitive Assessment (MoCa) and Addenbrooke’s Cognitive Examination-Revised (ACE-R) screening tools were used for cognitive status assessment and serum vitamin D levels analysis (blood samples of respondents). Significant difference (p = 0.022), was found in vitamin D levels in the alcohol-dependent group with cognitive deficiency 13.7 ± 9.4 (ng/mL), alcohol-dependent group without cognitive deficiency 19.5 ± 11.2 (ng/mL) and healthy controls 19.9 ± 11.1 (ng/mL), respectively. Furthermore, vitamin D levels were significantly different across all groups based on MoCa (p = 0.016) and ACE-R (p = 0.004) scores. All three groups exhibited vitamin D deficiency. A significant correlation was found between vitamin D deficiency and cognitive impairment, but it yielded no significant difference in alcohol-dependent individuals.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Association between Vitamin D and Cognitive Deficiency in Alcohol Dependence

et al. 2022

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“…Likewise, the subject has not been investigated in experimental animals treated with chronic ethanol. Only, it has been recently reported that Vit D deficiency may aggravate hepatic oxidative stress and inflammation in EtOH-treated rats [57].…”

Section: Discussionmentioning

confidence: 99%

The effect of 1,25-dihydroxyvitamin D3 on liver damage, oxidative stress, and advanced glycation end products in experimental nonalcoholic- and alcoholic- fatty liver disease

et al. 2021

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The effect of 1,25-dihydroxyvitamin D3 on liver damage, oxidative stress and advanced glycation end products in experimental nonalcoholic-and alcoholic-fatty liver disease Background/aim: Oxidative stress and advanced glycation end products (AGEs) formation are proposed as effective mechanisms in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). 1,25(OH)2D3 was proposed to have antioxidant, antiinflammatory and antiglycation properties. In this study, the effect of 1,25(OH)2 D3 treatment on oxidative stress parameters and AGEs levels together with hepatic histopathology was investigated in high fructose (HFr) or ethanol (EtOH)-treated rats. Materials and methods: Rats were treated with fructose (30%) or ethanol (5-20%) in drinking water with and without 1,25(OH)2D3 treatment (5 µg/kg two times a week) for 8 weeks. Insulin resistance (IR), oxidative stress parameters, AGEs, triglyceride (TG) and hydroxyproline (Hyp) levels together with histopathology were investigated in the liver. Results: 1,25(OH)2D3 decreased hepatic reactive oxygen species, lipid and protein oxidation products together with histopathological improvements in HFr-and EtOHtreated rats. 1,25(OH) 2 D 3 treatment was observed to decrease significantly serum and hepatic AGEs in HFr group, and hepatic AGEs in EtOH group. Conclusion: Our results clearly show that 1,25(OH)2 D3 treatment may be useful in the alleviation of hepatic lesions by decreasing glycooxidant stress in both NAFLD and ALD models created by HFr-and EtOH-treated rats, respectively.

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“…Di Luzio ( 1962) was the first to assume that ethanol could disrupt the oxidative balance of hepatic cells, either acting as prooxidants or reducing the antioxidant level eventually leading to necrosis or apoptosis (Hu et al, 2020). The process of apoptosis is critical in the development of liver disease.…”

Section: Discussionmentioning

confidence: 99%

γ‐Glutamylcysteine alleviates ethanol‐induced hepatotoxicity via suppressing oxidative stress, apoptosis, and inflammation

Liu

Lü

Zhang

et al. 2022

Journal of Food Biochemistry

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Alcohol abuse is a major cause of alcoholic liver disease (ALD) and can result in fibrosis and cirrhosis. γ-glutamylcysteine (γ-GC) is a precursor of glutathione (GSH) with antioxidant and anti-inflammatory properties. Our research aimed to explore the protective impact of γ-GC on ALD and its potential mechanisms of efficiency in vitro and in vivo. L02 cells were pretreated with γ-GC (20, 40, and 80 μM) for 2 h and exposed to ethanol for 24 h. Cell viability, apoptosis, oxidative stress, and inflammatory levels were measured. The expression of protein cleaved caspase-3 and cleaved PARP and flow cytometry results indicated that γ-GC decreases apoptosis on L02 cells after ethanol treatment. Moreover, γ-GC also attenuated oxidative stress and mitochondrial damage in hepatocytes caused by ethanol via increasing cellular GSH, SOD activity, and mitochondrial membrane potential. In vivo experiments, γ-GC effectively reduced the AST, ALT, and TG levels in mice. The inflammation of ALD was alleviated by γ-GC both in vivo and in vitro. Additionally, histopathological examination demonstrated that γ-GC treatment lessened lipid droplet formation and inflammatory damage. In conclusion, these results showed that γ-GC has anti-inflammatory and anti-apoptotic effects on ALD because it could help hepatocytes maintain sufficient GSH levels to combat the excess reactive oxygen species (ROS) generated during ethanol metabolism. Practical applicationsAlcohol intake is the fifth highest risk factor for premature death and disability among all risk variables. However, few medicines are both safe and effective for the treatment of ALD. As a direct precursor of GSH, γ-GC has a broad variety of potential antioxidant and anti-inflammatory applications for the treatment of numerous medical conditions. In conclusion, these results showed that γ-GC could protect cells from ALD via suppressing oxidative stress, alleviating inflammation, and preventing apoptosis.

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Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice

Cited by 15 publications

References 54 publications

Association between Vitamin D and Cognitive Deficiency in Alcohol Dependence

Association between Vitamin D and Cognitive Deficiency in Alcohol Dependence

The effect of 1,25-dihydroxyvitamin D3 on liver damage, oxidative stress, and advanced glycation end products in experimental nonalcoholic- and alcoholic- fatty liver disease

γ‐Glutamylcysteine alleviates ethanol‐induced hepatotoxicity via suppressing oxidative stress, apoptosis, and inflammation

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