Proliferación y apoptosis en epitelio lingual de ratones con tumores salivales inducidos por Dimetilbenzantraceno (DMBA) y modulados por lípidos dietarios
DOI:
https://doi.org/10.31053/1853.0605.v61.n2.33141Keywords:
Salivary glands, Tumors, Field cancerization, Dietary lipids, Cell proliferation, ApoptosisAbstract
Introductiomi: Aecorcling to the concept of fielcl defeets during the careinogenesis process, cxcessive cpithelial proliferation/ apoptosis may exist iii arcas near tunlors. Proliferation or apoptosis cou Id be mnodified by dietary lipids. Purpose: The present stucly vas designed ro analyze proltferation and apoptosis in tongue epitheliurn of inice Ucd cliets bascd nn different lipicls followed Uy induction of salivary tumors with DMBA. Mateninls and Methods: Forty-five clays after weaning, ten BALB/c mice were assigned to two chets: coro oil (CO) and fish oil (eod liver, FO). 'i\vo weeks later. DMBA vas injcctecl
in the submandibular area. Animals were sacrificed at the 13th post-in(ection weck. Sarnplcs of tongue were fixecl in formnalinethanol and irnmunohistocheinically stained for proliferation (Ki-67) and apoptosis (Bax). By light inicroseopv, the number of nuclei positive for these
niarkers were countcd out of three-hundred total interphase celis both in dorsal and in ventral tongue surfaces. Results were analyzed through Analysis of
Variance and t Test. Resu]ts: Cell proliferation vas greater in dorsal than in ventral tongue surfaces (p<0.0001) with no diet difference. Apoptosis was
significantly greater in mice fed FO than CO, particularly in tongue dorsal epithelia (p<O.Ol 8). Conclusions: This study shows that FO diet induces higher leveis of apoptosis in tongue epithelia suggesting a tissue defensive mechanism when exposed to a carcinogenic-tumoral agent
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