
Assessment of micronucleus frequency in the peripheral blood of female rats in persistent estrus treated with selective estrogen receptor modulators
2011; Wiley; Volume: 53; Issue: 1 Linguagem: Inglês
10.1002/em.20676
ISSN1098-2280
AutoresDorival Mendes Rodrigues‐Junior, Alesse Ribeiro dos Santos, Ana Amélia de Carvalho Melo Cavalcante, Airlane Pereira Alencar, Pedro Vitor Lopes‐Costa, Benedito Borges da Silva,
Tópico(s)Effects and risks of endocrine disrupting chemicals
ResumoAbstract The aim of this study was to evaluate micronucleus (MN) frequency in polychromatic erythrocytes (PCE) of female rats in persistent estrus (a model developed to mimic polycystic ovary syndrome) treated with selective estrogen receptor modulators (SERMs, tamoxifen, and raloxifene). Forty female Wistar‐Hannover rats were divided into four groups of 10 animals each: Group I (normally cycling rats) and Group II (persistent estrus) both received only vehicle, while Group III (persistent estrus) was treated with tamoxifen (250 μg/animal/day) and Group IV (persistent estrus) was treated with raloxifene (750 μg/animal/day). Tamoxifen and raloxifene were given by oral gavage beginning on postnatal day 90 and continuing for 30 consecutive days. Peripheral blood samples were collected from tails 1 day following the last exposure. Blood smears were made on glass slides and stained with 10% Giemsa solution. ANOVA and a Tukey post‐hoc test were used for data analysis. Mean percentages of MN were 1.82 ± 0.13, 5.20 ± 0.24, 3.32 ± 0.13, and 3.04 ± 0.12 in Groups I, II, III, and IV, respectively. The results indicate that tamoxifen and raloxifene similarly reduced the formation of MNPCE of female rats in persistent estrus ( P < 0.0001 for Groups III and IV vs. Group II), using the dosages and time periods applied in the present study. The data suggest possibly antimutagenic effects of SERMs under high levels of estrogens. The findings also suggest that this is an interesting animal model for studying the genotoxicity of estrogens. Environ. Mol. Mutagen. 2012. © 2011 Wiley Periodicals, Inc.
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