Effects of exposure to urban PM2.5 from air pollution in spermatogenesis of two generations of mice / Efeito da exposição ao material particulado (PM2,5) da poluição atmosférica na espermatogênese de duas gerações de camundongos

AUTOR(ES)
DATA DE PUBLICAÇÃO

2009

RESUMO

The present paper describes the effects of real exposure to urban PM2.5 on spermatogenesis by histological analysis of testes of mice (BALB/c) from two generations during fetal or postnatal phases of development and of mice exposed in both phases of development. Parental generations (BALB/c mice) were exposed to air pollution in chambers with or without filters for PM2.5 for 4 months (filtered and non-filtered chambers, respectively), forming two groups, namely non-exposed and exposed. These animals were mated and a frequency of decrease on vaginal plug in the exposed females was observed (p>0.05). The number of pregnant females was reduced as well (p=0.007) and the number of born alive decreased in the non-filtered chamber (186) when compared to the filtered chamber (268); however, the litter size was not altered (p>0.05). After mating, the male were killed, their testes were weighed and fixed in Bouins solution or 4% paraformaldehyde and stained in H&E, PCNA, Ki67 or TUNEL. Half of 1-day old offspring was crossed over between chambers forming the prenatal and postnatal groups; remaining offspring from filtered and non-filtered chambers comprised the non-exposed and pre+postnatally exposed groups, respectively. After 90 days, the animals from first generation were killed and their testes were removed, weighed, fixed and stained like the parental generation. The animals exposed to PM2.5 from the parental generation showed increased testis weight (p=0.002), epididymis weight (p<0.001), relative testis weight (p=0.003), and relative epididymis weight (p=0.001). The germ and somatic cells number was not reduced, and neither was cell proliferation (p>0.05). The apoptosis labeled by H&E was reduced in stage IV (p=0.046) and increased in stage VIII (p=0.019) of spermatogenesis. By using the TUNEL technique, stages IV (p=0.017), V (p=0.035) and VIII (p=0.024) showed fewer apoptosis in the exposed animal group. Stage IV was identified as the most spontaneous apoptosis in both methods: HE (p<0.001) and TUNEL (p<0.001), among the non-exposed animals. The cycle of the seminiferous epithelium was altered with reduced frequency of stage IV between the exposed animals (p=0.005). The animals from the first generation exposed during the prenatal period had a reduced body (p<0.001) and testis weight (p=0.012) and an increased relative testis weight (p=0.013). Differences in germ cell proliferation, apoptosis, and staging were not significantly different among treatment groups (p>0.05). Nevertheless, germ cell populations of post- (p=0.011) and pre+postnatally (p=0.035) PM-exposed animals contained an increased percentage of spermatocytes, while pre- and postnatal groups (p<0.001) had a reduced number of elongated spermatids. Stage IV was shown to be the most sensitive for the occurrence of spontaneous apoptosis in both methods used: H&E (p<0.001); and TUNEL (p<0.001). The normal frequency of the stages between non-exposed animals showed that the final stages are more frequent (VI, VIII e VII) and the beginning stages less frequent (II e I) to both generations. These results suggest that PM2.5 from urban air pollution is capable of altering the male reproductive system and spermatogenesis independently of the period of life when the animals are exposed to it (during or after pregnancy).

ASSUNTO(S)

camundongos spermatogenesis particulate matter air pollution espermatogênese poluição do ar material particulado

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