Oxidative stress in alcohol-induced rat parotid sialadenosis.
This study evaluated the effect of chronic ethanol consumption on the oxidative status of rat parotid and submandibular glands. To identify the endogenous response to ethanol ingestion, the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined. In addition, the antioxidant alpha-tocopherol was supplied to the animals in order to estimate its action in ethanol-associated glandular damage. The thiobarbituric acid reactive substances (TBARS), and the protein carbonyl (PC) content, both markers of cellular oxidative stress on lipid and protein structures, respectively, were recorded. Animals subjected to alcohol ingestion showed a low body growth rate with concomitant enlargement of absolute and relative parotid wet weight, compared with pair-fed calorie-controlled rats. Parotid glands of ethanol-treated animals showed increased SOD and GPx activity, and alpha-tocopherol was able to reduce their activities to the control levels. TBARS and PC were enhanced after chronic ethanol treatment in rat parotids. Supplemental alpha-tocopherol suppressed the oxidative ethanol-induced damage in lipid without affecting induced protein oxidation. Submandibular glands revealed no alterations in the weight, enzymatic and oxidative parameters tested due to ethanol and/or alpha-tocopherol ingestion. These findings indicate the involvement of oxidative stress in parotid gland sialadenosis due to ethanol consumption and the capability of alpha-tocopherol to halt lipid damage, although this low-molecular antioxidant compound leads to neither increased glandular weight nor protein oxidation in ethanol-induced parotid alterations.
Campos
Sara Cristina Gonçalves
SC
Departamento de Ciências Exatas, Escola de Farmácia e Odontologia de Alfenas, Alfenas, MG, Brazil.
Moreira
Denise Aparecida Corrêa
DA
Nunes
Terezinha D'Avila e Silva
TD
Colepicolo
Pio
P
Brigagão
Maísa Ribeiro Pereira Lima
MR
D000437:Alcoholism / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress; D010305:Parotid Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013363:Submandibular Gland / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism; D024502:alpha-Tocopherol / Q000494:pharmacology
D000975:Antioxidants; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D024502:alpha-Tocopherol