The effect of chronic alcohol intoxication and smoking on the activity of oral peroxidase

Abstract

Abstract:Peroxidase is the most important antioxidant enzyme in saliva. Through peroxidation of thiocyanate in the presence of H 2 O 2 , peroxidase catalyses the formation of bacteriocidic compounds such as hypothiocyanate. The purpose of this study was to evaluate the effect of chronic alcohol intoxication and smoking on the activity of oral peroxidase (OPO). A total of 37 volunteers participated in the study. This cohort consisted of 17 male alcohol-dependent smoking patients after chronic alcohol intoxication (AS group, alcohol + smoking) (mean age: 42 years; range: 26-55) (100-700 g/day of alcohol; 10-20 cigarettes/day) and 20 control male social drinkers (CNS group, control non-smokers) with no history of alcohol abuse or smoking (mean age: 42 years; range: 30-53). Salivary peroxidase activity was measured by the colorimetric method. The differences between groups were evaluated using the Mann-Whitney U test. There was significantly higher activity of OPO (p = 0.00001) and significantly lower salivary flow (SF) (p = 0.007) in alcohol-dependent smokers after chronic alcohol intoxication compared to the control group. OPO activity significantly correlated with the number of days of alcohol intoxication, but not with smoking. Gingival index (GI) was significantly higher in smoking alcohol-dependent persons than in the control group, and correlated with OPO activity. The sensitivity of the OPO test was 70% in smoking alcoholics, while specificity was 95%. The increased activity of OPO suggests chronic oxidative stress is more likely due to ethanol action than to smoking. Smoking alcohol-dependent persons have a worse periodontal status than controls. OPO activity as a marker of chronic alcohol abuse may help in the diagnosis of alcoholism.

Salivary lysozyme in smoking alcohol dependent persons

“…In alcohol abusers and smokers, there have been reported disturbed function of the salivary glands with concomitant decrease in the secretion of salivary proteins, impairment in the immune mechanisms such as phagocytosis, chemotaxis, increased production of peroxides, and impaired function and proliferation of B and T lymphocytes and production of immunoglobulins [3,8,15]. People who chew tobacco have decreased levels of lysozyme and lactoferrin and increased secretion of immunoglobulin A in their saliva [9,10], which indicates reduced innate and activated acquired immunity of the saliva. Persons addicted to alcohol have been reported to have lower output of lactoferrin (non-smokers) [10] and immunoglobulin A (smokers) [9], which, together with the reduced output of lysozyme in our study, indicated suppression of immunity mediators present in the saliva.…”

“…People who chew tobacco have decreased levels of lysozyme and lactoferrin and increased secretion of immunoglobulin A in their saliva [9,10], which indicates reduced innate and activated acquired immunity of the saliva. Persons addicted to alcohol have been reported to have lower output of lactoferrin (non-smokers) [10] and immunoglobulin A (smokers) [9], which, together with the reduced output of lysozyme in our study, indicated suppression of immunity mediators present in the saliva. Generally, both alcohol abuse and cigarette smoking produce a synergistic increase in the concentration of acetaldehyde in the saliva [9].…”

“…Smoking is usually associated with poor oral hygiene and a heavier course of periodontitis than non-smoking [11]. Similarly to alcohol, cigarette smoke is a source of oxidative stress and increased concentrations of acetaldehyde in the oral cavity [8][9][10][11]. In alcohol abusers and smokers, there have been reported disturbed function of the salivary glands with concomitant decrease in the secretion of salivary proteins, impairment in the immune mechanisms such as phagocytosis, chemotaxis, increased production of peroxides, and impaired function and proliferation of B and T lymphocytes and production of immunoglobulins [3,8,15].…”

“…Acute local mucosa damage is reversible and proportional to the quantity and concentration of alcohol. Ethanol immediately diffuses into the saliva and oral tissues, reaching even higher concentrations than in plasma [8][9][10]. Acetaldehyde and reactive oxygen species derived from alcohol and tobacco smoke are widely known factors of tissue damage and carcinogenesis.…”

Effects of Daily Alcohol Intake on Serum and Salivary Alpha-Amylase Activity Associated With Two Local Alcoholic Drinks of Benin

“…The increased activity of lysosomal glycosidases in the saliva of alcoholics is attributable to ethanol itself as well as alcohol metabolites, and may occur via many mechanisms: increased lysosomal membrane permeability, delayed removal of the enzymes from saliva, impaired trafficking of lysosomal hydrolases to organelles, enhanced synthesis of enzyme by activated leucocytes or leakage from damaged cells (Waszkiewicz et al, 2013). Therefore, in alcoholics, lysosomal and cellular membranes of the oral cavity tissues (including oral mucosa and salivary glands) may be damaged, and proteases together with glycosidases (including alpha amylase) may be transferred to cytosol, extracellular matrix, and to saliva (Waszkiewicz et al, 2012). To the contrary, some authors have noted a reduction in the activity of salivary alpha-amylase in case of acute administration of alcohol (Enberg et al, 2001;Rohleder and Nater, 2009).…”