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Magnesium, Calcium, Potassium, Sodium, Phosphorus, Selenium, Zinc, and Chromium Levels in Alcohol Use Disorder: a Review

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Journal of Clinical Medicine Review Magnesium, Calcium, Potassium, Sodium, Phosphorus, Selenium, Zinc, and Chromium Levels in Alcohol Use Disorder: A Review Jacek Baj 1,* , Wojciech Flieger 2, Grzegorz Teresi´nski 3, Grzegorz Buszewicz 3 , El˙zbietaSitarz 4 , Alicja Forma 3 , Kaja Karakuła 4 and Ryszard Maciejewski 1 1 Chair and Department of Anatomy, Medical University of Lublin, 20-090 Lublin, Poland; [email protected] 2 Faculty of Medicine, Medical University of Lublin, Aleje Racławickie 1, 20-059 Lublin, Poland; [email protected] 3 Chair and Department of Forensic Medicine, Medical University of Lublin, 20-090 Lublin, Poland; [email protected] (G.T.); [email protected] (G.B.); [email protected] (A.F.) 4 Chair and 1st Department of Psychiatry, Psychotherapy and Early Intervention, Medical University of Lublin, Gluska Street 1, 20-439 Lublin, Poland; [email protected] (E.S.); [email protected] (K.K.) * Correspondence: [email protected] Received: 27 May 2020; Accepted: 15 June 2020; Published: 18 June 2020 Abstract: Macronutrients and trace elements are important components of living tissues that have different metabolic properties and functions. Trace elements participate in the regulation of immunity through humoral and cellular mechanisms, nerve conduction, muscle spasms, membrane potential regulation as well as mitochondrial activity and enzymatic reactions. Excessive alcohol consumption disrupts the concentrations of crucial trace elements, also increasing the risk of enhanced oxidative stress and alcohol-related liver diseases. In this review, we present the status of selected macroelements and trace elements in the serum and plasma of people chronically consuming alcohol. Such knowledge helps to understand the mechanisms of chronic alcohol-use disorder and to progress and prevent withdrawal effects, also improving treatment strategies. Keywords: alcoholism; alcohol use disorder; zinc; chromium; selenium; calcium; potassium; magnesium; phosphorous; sodium 1. Introduction Alcohol dependence among adults in the United States is estimated at 14% [1]. Among heavy drinkers, alcoholic liver disease is estimated to develop in 15–30% [2]. In patients who consume excessive amounts of alcohol, various types of disturbances are observed, i.e., electrolyte, acid-base, protein-caloric malnutrition, and vitamin deficiency [3–5]. Chronic alcohol abuse patients are malnourished not only because of a diet low in nutrients but also because alcohol impairs the absorption of essential nutrients and elements. In addition, ethanol metabolic pathways produce toxic metabolites (acetaldehyde and free radicals) that lead to cell damage as a result of oxidative stress [6,7]. The clinical picture of the observed disorders depends on the duration and amount of alcohol consumed. Most patients who develop electrolyte imbalance, metabolic acidosis, and hyponatremia are admitted to hospital. However, clinical symptoms of chronic alcohol consumption are also decreased levels of phosphate, magnesium, potassium, sodium and calcium, and other elements in blood plasma [8–10]. Electrolyte abnormalities develop as a result of chronic alcohol consumption during acute alcohol intoxication, but they are particularly important during alcohol withdrawal [11–14]. J. Clin. Med. 2020, 9, 1901; doi:10.3390/jcm9061901 www.mdpi.com/journal/jcm J. Clin. Med. 2020, 9, x FOR PEER REVIEW 2 of 23 J. Clin. Med. 2020, 9, 1901 2 of 24 during acute alcohol intoxication, but they are particularly important during alcohol withdrawal [11–14]. It turns out that even during alcohol withdrawal, hypokalemia, hypomagnesemia, and It turns out that even during alcohol withdrawal, hypokalemia, hypomagnesemia, and hyponatremia hyponatremia are observed [15,16]. are observed [15,16]. Currently, it is believed that the toxic effects of alcohol on organs are mainly associated with the Currently, it is believed that the toxic effects of alcohol on organs are mainly associated with the activity of alcohol metabolites, induction of oxidative stress, and translocation of intestinal activity of alcohol metabolites, induction of oxidative stress, and translocation of intestinal endotoxins endotoxins into the bloodstream [17–20]. These processes lead to cell damage and stimulation of into the bloodstream [17–20]. These processes lead to cell damage and stimulation of inflammatory inflammatory reactions releasing a large number of cytokines, among others such as TNF-alpha and reactions releasing a large number of cytokines, among others such as TNF-alpha and IL-6 [21,22]. IL-6 [21,22]. With continuous alcohol abuse, which stimulates hepatocytes to secrete some With continuous alcohol abuse, which stimulates hepatocytes to secrete some interleukins, such as IL-8, interleukins, such as IL-8, activating Kupffer cells by binding to toll-like receptors, other effects are activating Kupffer cells by binding to toll-like receptors, other effects are impaired including defective impaired including defective tissue regeneration, hepatocyte necrosis, recruitment of neutrophils tissue regeneration, hepatocyte necrosis, recruitment of neutrophils and immune cells, and liver and immune cells, and liver fibrosis [23]. fibrosis [23]. Alcohol is metabolized in three pathways, involving enzymes such as the alcohol Alcohol is metabolized in three pathways, involving enzymes such as the alcohol dehydrogenase dehydrogenase present in the cytosol, the Microsomal Ethanol Oxidizing System (MEOS), and the present in the cytosol, the Microsomal Ethanol Oxidizing System (MEOS), and the catalase (CAT) catalase (CAT) contained in peroxisomes (Figure 1). contained in peroxisomes (Figure1). Figure 1. Three pathways of alcohol metabolism. Figure 1. Three pathways of alcohol metabolism. Each of the three pathways is responsible for the production of free radicals [24], which can damage lipids,Each proteins, of the carbohydrates, three pathways and is responsible DNA substrates for the [25 production]. However, of there free areradicals several [24], endogenous which can enzymesdamage lipids, that protect proteins, the bodycarbohydrates, against the and adverse DNA effsubstratesects of free [25]. radicals, However, including there glutathioneare several peroxidaseendogenous (GPx), enzymes which that neutralizes protect the hydrogen body against peroxide the and adverse organic effects peroxides, of free glutathione radicals, reductaseincluding (GR),glutathione superoxide peroxidase dismutase (GPx (SOD)), which and CAT neutralizes [26]. Cofactors hydrogen for antioxidant peroxide enzymes and organic are trace peroxides, elements suchglutathione as selenium, reductase manganese, (GR), superoxide copper, zinc, dismutase and iron. Selenium(SOD) and in CAT the form [26]. of Cofactors selenocysteine for antioxidant is present inenzymes the active are center trace ofelements GPx. In such turn, as manganese, selenium, copper,manganese, and zinc copper, are components zinc, and iron. of the Selenium enzymes in from the theform superoxide of selenocysteine dismutase is grouppresent (MnSOD, in the active Cu/ZnSOD), center of which GPx. catalyzeIn turn, themanganese, reaction ofcopper, the superoxide and zinc anionare components radical dismutation of the enzymes to hydrogen from the peroxide superoxide and oxygen.dismutase Iron group is a part(MnSOD of CAT, Cu/ZnSOD that catalyzes), which the decompositioncatalyze the reaction of hydrogen of the superoxide peroxide into anion water radical and dismutation oxygen. Zinc-dependent to hydrogen peroxide enzymes, and in turn, oxygen. are alcoholIron is a dehydrogenase, part of CAT that RNA catalyzes polymerases, the decomposition and fructose of hydrogen 1,6-bisphosphatase, peroxide into which water is allosterically and oxygen. regulatedZinc-dependent by zinc enzymes, and could in influenceturn, are gluconeogenesis.alcohol dehydrogenase, Therefore, RNA trace polymerases, element concentrations and fructose have1,6-bisphosphatase, a significant impact which on is theallosterically activity of regulated antioxidant by enzymes,zinc and could and thus, influence on the gluconeogenesis. modulation of ethanol-inducedTherefore, trace oxidativeelement concentrations stress. Research have to date a significant has shown impact that alcoholism on the activity significantly of antioxidant changes macroelementenzymes, and homeostasis,thus, on the i.e.,modulation calcium, of phosphorous, ethanol-induced magnesium, oxidative sodium, stress. potassium,Research to and date trace has minerals,shown that which, alcoholism as cofactors significantly for antioxidant changes enzymes,macroelement play ahomeostasis, role in the fight i.e., against calcium, oxidative phosphorous, stress andmagnesium, may affect sodium, survival potassium, (Table1). and trace minerals, which, as cofactors for antioxidant enzymes, play a role in the fight against oxidative stress and may affect survival (Table 1). J. Clin. Med. 2020, 9, 1901 3 of 24 Table 1. Minerals deficiency in patients of alcohol abuse. Sample Concomitant Diseases Patients Determined Element Results of Other Measured Parameters/Treatment Ref. Source -the low serum zinc group had the higher AST: ALT ratio, 40% of subjects had low serum without 108 (male and female) the lower albumin levels, and the higher CRP, lower bilirubin [27] Zn levels levels. -albumin, transferrin, and prealbumin were depressed in serum without 7 patients low Zn levels [28] zinc-deficient patients. lower Zn in AD + HIV serum HIV infection 7 (AD + HIV), 7 (AD) -AD + HIV: elevation
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