Trace Element Levels and Oxidant/Antioxidant Status in Patients with Alcohol Abuse

Sarıbal, Devrim; Hocaoglu-Emre, Fatma Sinem; Karaman, Fulya; Mirsal, Hasan; Akyolcu, Mehmet Can

doi:10.1007/s12011-019-01681-y

Cited by 22 publications

(21 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is a prerequisite to proposing rational intervention in clinical practice. Several reviews of metallomics in the context of alcoholism have appeared in recent years [ 13 , 15 , 17 , 27 , 47 , 48 , 51 , 52 ]. However, there are still many limitations to the research undertaken related to the small sample size, discrepancies in the measurement techniques used, the lack of homogeneity of the samples, etc.…”

Section: Discussionmentioning

confidence: 99%

“…Chronic alcohol consumption disturbs the electrolyte balance and the levels of trace elements in the serum and tissues, mainly as a result of gastrointestinal dysfunction and malabsorption, which is reflected in general malnutrition [ 13 , 14 ]. A number of reports describe disturbances in the concentration of trace elements in various tissues as a result of chronic alcohol consumption [ 15 , 16 ]. The most frequently reported abnormalities are iron overload, hypomagnesemia, and selenium and zinc deficiency.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Chronic Alcohol Abuse Alters Hepatic Trace Element Concentrations-Metallomic Study of Hepatic Elemental Composition by Means of ICP-OES

et al. 2022

View full text Add to dashboard Cite

Trace element accumulation varies in different human tissues. Distribution of several elements was found to be disrupted in the case of excessive alcohol consumption, causing negative effects and exacerbation of pathological processes in the liver. In this study, we analyzed the levels and interactions between seven trace elements including calcium (Ca), cobalt (Co), chromium (Cr), copper (Cu), iron (Fe), potassium (K), and magnesium (Mg), manganese (Mn), sodium (Na), zinc (Zn), and selenium (Se) in individuals with alcohol-use disorder (AUD) and patients without AUD (control group). The liver samples were collected during autopsy from 39 individuals with AUD and 45 control subjects. Elemental composition inductively coupled plasma optical emission spectrometry (ICP-OES) after wet mineralization by nitric acid was applied for the evaluation of the samples. Positive correlations dominated in the AUD group, mainly in relation to Mg, which strongly positively correlated with Ca, Mn, Fe; K correlated with Mn and Zn, and Cu positively correlated with K and Zn. The strongest positive correlation in the AUD group was observed for the Mg-Mn pair (r = 0.87). Significant statistical differences (p < 0.05) between the groups concerned the average concentration of Co, Cu, Mn, and Mg, which were lower in the AUD group, and Fe, the level of which was significantly higher in the AUD group compared to the control group. Evaluation of the chronic alcohol consumption effect on the accumulation of trace elements in the liver allows a better understanding of the pathological processes taking place in this organ.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic Alcohol Abuse Alters Hepatic Trace Element Concentrations-Metallomic Study of Hepatic Elemental Composition by Means of ICP-OES

et al. 2022

View full text Add to dashboard Cite

show abstract

“…SOD balances ROS by scavenging free radicals and prevents cell damage caused by superoxide anion radicals (18). Moreover, MDA is a widely detected oxidative damage marker and elevated MDA levels are the result of lipid peroxidation (19). SOD levels are negatively correlated with MDA levels and the quantification of SOD and MDA levels can infer the metabolism of free radicals, which therefore reflects the degree of oxidative stress in the cells (32).…”

Section: Discussionmentioning

confidence: 99%

“…As MDA is a widely detected marker of oxidative damage and its elevated level is the result of lipid peroxidation (19), MDA levels in HeLa cells were determined using the thiobarbituric acid method. Cells were inoculated at a density of 5x10 5 cells/ml in 6-well plates and were cultured in an incubator at 37˚C with 5% CO 2 for 24 h. Following centrifugation at 200 x g for 10 min at room temperature, the supernatant was discarded and the cells were treated as the control group or with LPA, DOX or LPA + DOX for 24 h at 37˚C.…”

Section: Mda Detectionmentioning

confidence: 99%

Lysophosphatidic acid protects cervical cancer HeLa cells from apoptosis induced by doxorubicin hydrochloride

Wang

Mou

et al. 2022

Oncol Lett

View full text Add to dashboard Cite

Cervical cancer is one of the most common types of gynecological tumors. Lysophosphatidic acid (LPA), as a bioactive lipid medium, plays an important role in numerous physiological and pathophysiological processes, including the stimulation of cell migration and tumor cell invasion. LPA is increased in the plasma of patients with cervical cancer. Doxorubicin hydrochloride (DOX) is used as a first-line drug in the treatment of cervical cancer in clinics, however, the effect and molecular mechanism of LPA on DOX-induced apoptosis in cervical cancer cells remain unclear. Therefore, the present study aimed to explore the effect and underlying molecular mechanism of LPA on DOX-induced apoptosis in cervical cancer cells. HeLa cells were treated as a control group or with LPA (10 µmol/l), DOX (4 µmol/l) or LPA (10 µmol/l) + DOX (4 µmol/l) for 24 h. Using transmission electron microscopy the results demonstrated that LPA reduced cell death and the degree of chromatin aggregation in DOX-induced HeLa cells. Reverse transcription-quantitative PCR demonstrated that LPA significantly downregulated caspase-3 mRNA expression levels in DOX-induced HeLa cells. Moreover, western blotting demonstrated that LPA significantly reduced caspase-3 and cleaved caspase-3 protein expression levels in DOX-induced HeLa, C33A and SiHa cells. Furthermore, flow cytometry demonstrated that LPA may prevent apoptosis in DOX-induced HeLa cells (P<0.05).Using dichloro-dihydro-fluorescein diacetate assay, it was demonstrated that LPA significantly reduced the intracellular ROS levels induced by DOX. In summary, the present study indicated that LPA may protect HeLa cells from apoptosis induced by DOX. These findings have provided experimental evidence that LPA may be a potential therapeutic target for the treatment of cervical cancer.

show abstract

“…Reduced serum levels of trace elements have been confirmed in patients with liver disease, including ALD, and correlate with severity[ 107 - 110 ]. Decreased zinc is associated with liver cirrhosis in alcohol dependent individuals[ 111 ] and reduced serum levels of zinc, copper and iron have been observed when compared with healthy controls[ 112 ]. Zinc is a crucial trace element involved in multiple cellular and metabolic pathways[ 113 ] as well as acting as a cofactor for ALDH.…”

Section: Trace Elementsmentioning

confidence: 99%

Oxidative stress in alcohol-related liver disease

Tan

Yates

Lilly

et al. 2020

WJH

102

View full text Add to dashboard Cite

Alcohol consumption is one of the leading causes of the global burden of disease and results in high healthcare and economic costs. Heavy alcohol misuse leads to alcohol-related liver disease, which is responsible for a significant proportion of alcohol-attributable deaths globally. Other than reducing alcohol consumption, there are currently no effective treatments for alcohol-related liver disease. Oxidative stress refers to an imbalance in the production and elimination of reactive oxygen species and antioxidants. It plays important roles in several aspects of alcohol-related liver disease pathogenesis. Here, we review how chronic alcohol use results in oxidative stress through increased metabolism via the cytochrome P450 2E1 system producing reactive oxygen species, acetaldehyde and protein and DNA adducts. These trigger inflammatory signaling pathways within the liver leading to expression of pro-inflammatory mediators causing hepatocyte apoptosis and necrosis. Reactive oxygen species exposure also results in mitochondrial stress within hepatocytes causing structural and functional dysregulation of mitochondria and upregulating apoptotic signaling. There is also evidence that oxidative stress as well as the direct effect of alcohol influences epigenetic regulation. Increased global histone methylation and acetylation and specific histone acetylation inhibits antioxidant responses and promotes expression of key pro-inflammatory genes. This review highlights aspects of the role of oxidative stress in disease pathogenesis that warrant further study including mitochondrial stress and epigenetic regulation. Improved understanding of these processes may identify novel targets for therapy.

show abstract

Trace Element Levels and Oxidant/Antioxidant Status in Patients with Alcohol Abuse

Cited by 22 publications

References 32 publications

Chronic Alcohol Abuse Alters Hepatic Trace Element Concentrations-Metallomic Study of Hepatic Elemental Composition by Means of ICP-OES

Chronic Alcohol Abuse Alters Hepatic Trace Element Concentrations-Metallomic Study of Hepatic Elemental Composition by Means of ICP-OES

Lysophosphatidic acid protects cervical cancer HeLa cells from apoptosis induced by doxorubicin hydrochloride

Oxidative stress in alcohol-related liver disease

Contact Info

Product

Resources

About