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1.
IJRM-Iranian Journal of Reproductive Medicine. 2012; 10 (1): 7-14
in English | IMEMR | ID: emr-117347

ABSTRACT

Phthalate esters have been shown to cause reproductive toxicity in both developing and adult animals. This study was designed to assess long-term effects of maternal exposure to Di [2-ethylhexyl] Phthalate [DEHP] on reproductive ability of both neonatal and adult male offspring. 60 female rats randomly divided in four equal groups; vehicle control and three treatment groups that received 10, 100 and 500 mg/kg/day DEHP via gavage during gestation and lactation. At different ages after birth, the volumes of testes were measured by Cavellieri method, testes weights recorded and epididymal sperm samples were assessed for number and gross morphology of spermatozoa. Following tissue processing, seminiferous tubules diameter and germinal epithelium height evaluated with morphometric techniques. Mean testis weight decreased significantly [p<0.05] in 500 mg/kg/day dose group from 28 to 150 days after birth. Significant decreases were seen in total volumes of testis in 100 [p<0.05] and 500 [p<0.01] mg/kg/day doses groups until 150 days after birth. Seminiferous tubules diameter and germinal epithelium height decreased significantly in 100 [p<0.05] and 500 [p<0.01] mg/kg/day doses groups during postnatal development. Also, mean sperm density in 100 mg/kg/day [p<0.05] and 500 mg/kg/day [p<0.01] doses groups and percent of morphologically normal sperm in highest dose group [p<0.05] decreased significantly until 150 days after birth. Present study showed that maternal exposure to Di [2-ethylhexyl] Phthalate during gestation and lactation caused to permanent and dose-related reductions of sperm and testicular parameters in rats offspring


Subject(s)
Animals , Female , Testis/drug effects , Spermatozoa/drug effects , Prenatal Exposure Delayed Effects , Reproduction/drug effects , Rats, Wistar , Gene Expression/drug effects
2.
IJFS-International Journal of Fertility and Sterility. 2011; 5 (1): 39-46
in English | IMEMR | ID: emr-110544

ABSTRACT

During the last decades, environmental contamination by lead generated from human activities has become an evident concern. The present study assessed the long-term effects of neonatal exposure to different doses of lead acetate on the ovaries of offspring rats. Pregnant female Wistar rats were randomly divided into a control and three experimental groups. The experimental groups received 20, 100 and 300 mg/L/day lead acetate via drinking water during lactation. Ovaries of the offspring were removed at 30, 60, 90 and 120 days of age, their weights recorded and fixed in Bouin's solution. Following tissue processing, 5 micro m serial sections were stained with hematoxylin-eosin, and then, the numbers and diameters of ovarian follicles and corpora lutea were estimated. Ovary weights decreased significantly [p<0.05] in the 300 mg/L/day dose groups at 30, 60 and 90 days postnatal development. Significant dose-related decreases were seen in the numbers of primary, secondary and antral follicles in 100 [p<0.05] and 300 mg/L/day doses groups at 30 and 60 days of age [p<0.01]. There was significant decrease in mean number of corpora lutea in the 100 [p<0.05] and 300 [p<0.01] mg/L/day dose groups at 60 days of age. It seems that neonatal lead treatment has transient effects on follicular development in the ovary of offspring and ovarian parameters gradually improve until 90 days of age. The present study showed that maternal lead acetate exposure affects prepubertal ovarian follicle development in a dose dependent manner, but ovarian parameters gradually improve during the postpubertal period


Subject(s)
Female , Animals, Laboratory , Organometallic Compounds , Lead , Rats, Wistar , Random Allocation , Lactation , Ovarian Follicle/growth & development , Infertility , Infant, Newborn/growth & development , Ovary/growth & development
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