RESUMO
OBJECTIVE: The purpose of the present study is to evaluate the relationships between occupational exposure to mine dust, salivary antioxidants and their possible implications in the pathogenicity of different exposure diseases. MATERIAL AND METHODS: We studied 30 individuals with long-term occupational exposure to non-ferrous metal mine conditions and a control group consisted of 30 healthy volunteers. Salivary uric acid, gammaglutamyltransferase (GGT), albumin and the total antioxidant capacity (TAC) were measured. RESULTS: Statistically significant differences in salivary GGT (P = 0.004), TAC (P < 0.001) and uric acid (P = 0.02) were noted between the two groups. A strong positive correlation between TAC and uric acid was recorded in controls (r = 0.76, P = 0.0002). CONCLUSIONS: Saliva may provide an important line of antioxidant defense in humans exposed to oxidant threats. These components may also serve as convenient biomarkers to monitor oxidant exposure.
Assuntos
Antioxidantes/análise , Metais , Mineração , Saliva/química , Adulto , Albuminas/análise , Benzotiazóis , Biomarcadores/análise , Compostos Cromogênicos , Colorimetria/métodos , Poeira , Humanos , Indicadores e Reagentes , Pessoa de Meia-Idade , Exposição Ocupacional , Projetos Piloto , Romênia , Proteínas e Peptídeos Salivares/análise , Ácidos Sulfônicos , Ácido Úrico/análise , Ácido Úrico/sangue , gama-Glutamiltransferase/análiseRESUMO
Smoking, one of the avoidable causes of mortality, is considered a major risk factor for cardiovascular diseases, chronic obstructive pulmonary diseases, and bronchopulmonary cancer. Many studies suggest that nicotine induces vasoconstriction, not only in coronary arteries but also in peripheral vessels, hypertension, pro-atherogenic effects, due to increase of platelet activation and fatty acids concentration, alterations of endothelial-cell shapes, as well as endothelial-cell proliferation. The main affected vascular biochemical parameters are: endothelin-1, cholesterol, triglycerides, lipoproteins, C-reactive protein, nitric oxide, fibrinogen, and uric acid. Cigarette smoke induces inflammation in respiratory epithelium, through local irritation due to release of oxidants, aldehydes, acids, ammonium; impaired ciliar function, and retention of mucus and toxins, followed by infection; carcinogenesis due to oncogene-expression induced by oxidants, aromatic hydrocarbons, and nitrosamines. These effects are induced by alterations of endothelin-1, nitric oxide, IL1, IL6, TNF, and the CYP Enzyme System. Saliva is the first biological fluid encountered by the cigarette smoke. In vitro and in vivo salivary exposure to cigarette smoke has been shown to determine changes of concentrations of lactate dehydrogenase, amylase, and uric acid, in saliva--important factors of the antioxidant salivary system. Such changes may promote occurrence of upper digestive cancers.