The purpose of this study was to clarify the effects of long-term ethanol and acetaldehydeconsumption on histopathological changes in rat tongue epithelium.
One hundredeight male Wistar rats (300g body weight) were divided into 4 groups. The ethanol group (n=29) was given a 5% ethanol diet (ORIENTAL YEAST). The control group (n=33) was fed a control diet (ORIENTAL YEAST). Moreover, the tongue epithelium was coated daily with acetaldehyde (AA) at a concentration of 180m M in the daily AA (n=22) and ethanol+ AA groups (n=24). Animals were killed after 24 weeks. Their tongues were removed, and dorsal, lateral, and sublingual sites. Were studied histologically by H-E staining, histochemical anti-PCNA staining, and SEM.
In the AA and ethanol+AA groups, the keratic thickness of the dorsal and sublingual sites had significantly increased (AA: p<0.05, ethanol+ AA: p<0.01, vs control and Ethanol groups). Epithelial thickness and cell number in the three sites did not significantly differ among the groups. In the ethanol, AA, and ethanol+AA groups, PCNA positive cells in the basal layer increased considerably (p<0.01, vs control group). Moreover, in the AA and ethanol+AA groups, PCNA-positive cells in the lower 1/3 of the epithelial layers significantly increased (p<0.01, vs control and ethanol groups). Nine cases of hyperkeratosis were found at the dorsal prominence of the tongue, 1 in the ethanol group (3.4%), 2 in the AA group (9.1%) and 6 in the ethanol+ AA group (25.0%).
Acetaldehyde, a primary metabolite of ethanol may play a direct role in the pathogenesis of tongue cancer in the rat.
