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Polychlorinated Biphenyls (Aroclor 1254) on Reproductive Toxicology in Mice

Author: MaBaoHua
Tutor: ShiZhiCheng;WangJianHua
School: Northwest University of Science and Technology
Course: Clinical Veterinary Medicine
Keywords: Aroclor 1254 PCBs Reproduction Toxicology Mice
CLC: S859.8
Type: PhD thesis
Year: 2003
Downloads: 405
Quote: 3
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Abstract


Mouse animal models to study the typical representative of the substance - of Aroclor 1254 on maternal oogenesis, fertilization and preimplantation embryos in vivo developmental toxicity, male mouse spermatogenesis toxicity of dioxin-like PCBs and sperm fertilizing capacity the fertilized egg vivo developmental toxicity. The combination of the ovaries and uterus, testis and epididymis histopathological study to analyze the possible mechanism of toxicity. Research using Aroclor 1254 standard sterilization peanut oil dilution after intraperitoneal injection of doses of 1/10, 1/50, 1/250 and 1/1250 LD 50 , control group was injected peanut oil. To sexual maturity, weaning female rats and male mice exposed to make direct contact with Aroclor 1254; lactating female rats and pregnancy maternal exposure, and the the lactating pups and fetal indirect contact Toxicity of the aroclor 1254. With increasing doses of exposure to maternal ovulation rate of Aroclor 1254 showed a downward trend during the period, including sexual maturity and fetal period came into contact with a number of 1/10 LD 50 Aroclor 1254 maternal ovulation decreased significantly, the fertilization rate of the different experimental mice with no significant difference between the control group. Ovarian histopathological observation that the reduction in the number of maternal ovulation atresia degradation due to the process of follicular development. Oocytes can complete the fertilization process, most of the fertilized egg can complete the first cleavage, and development to the 2 - cell embryo. Sexual maturity and fetal period came into contact with 1/10 LD 50 Toxicity of the aroclor 1254 dams oocyte fertilization rate was significantly decreased, different experimental group mothers fertilization rate with no significant difference between the control group. The Aroclor 1254 toxic effect mainly in the 2 - cell embryos further development process of embryonic development to the morula and blastocyst rate decreased significantly with increasing doses of embryos and degeneration embryo developmental delay ratio increased significantly. The main reason is that the structure of the Aroclor 1254 direct toxic effects and genital abnormalities, inflammatory response and pathological changes of cells, can not support normal embryonic development, cleavage - cell embryo development to the morula and blastocyst affected, resulting in arrested development or degeneration. In addition, the affected female rats during the embryonic development of ovarian follicular development and luteal stunting embryonic development is blocked and developmental degradation may constitute part of the reason. Due to the toxic effects of Aroclor 1254, leading to sexual maturity in male rats, testicular structure and cell lesions of spermatogenesis mainly spherical sperm cell development and sperm maturation process. With increasing doses of sperm motility was significantly decreased abnormal sperm and abnormal sperm acrosome ratio significantly increased to a lesser extent by the impact of sperm density. Weaning period came into contact with the direct toxic effects of Aroclor 1254 and the resulting gonadal lesions, material storage and meiosis, spermatocytes and spherical sperm cell development and sperm final maturation process, so that 1/10 LD 50 exposed groups of male mice sperm density significantly reduced with increased doses of sperm motility significantly reduce a significant increase in abnormal sperm and abnormal sperm acrosome ratio. Lactation and fetal life came into contact with Aroclor 1254 male mouse germ cell proliferation and spermatocytes material storage obstacles that reduced the number of germ cells matured sperm density decreased significantly with increasing doses of. Due to the relatively low amount of the fetus and the offspring Aroclor 1254 transit through the placenta and breast milk, did not cause significant pathological changes of the gonads, the quality of sperm morphology are affected significantly reduced. With sexual maturity contact Aroclor 1254 male rats not normal female rats exposed to breeding research results show that the Aroc lor 1254 mouse reproductive toxicology studies with the increase in male rats exposed to doses of fertilization rate and zygote The first cleavage rate and delay. Still developmental delay and developmental degradation morula embryos and blastocysts was significantly lower in the further development of 2-cell embryos. The different periods of the main conclusions: (1) for the first time systematically from sexual maturity, weaning, lactation and fetal periods of ontogeny, mice with different doses of contact AroClor 1254, studied Aroc1oI '1254 on mother mouse oogenesis, fertilization and preimplantation embryo in vivo development, as well as the male mouse spermatogenesis toxicology. (2) for the first time, the number of ovulation, fertilization rate, the first cleavage rate of fertilized eggs, embryo development rate of morula, blastocyst hatched of embryo development rate, and developmental delay embryo degeneration The ratio of the embryo, different periods of ontogeny contact with different doses of AroClor 1254 mouse oogenesis, fertilization and preimplantation embryo developmental toxicity in vivo system quantitatively. That affected maternal oogenesis, fertilization and embryonic development toxicity of a dose-response relationship, and the effect of the characteristics associated with ontogenetic stage. (3) for the first time an individual from different developmental exposure to Aroclor 1254 maternal ovarian, uterine histopathological findings on oogenesis, fertilization and preimplantation embryo developmental toxicity in vivo mechanism qualitative. Prove the mature follicular development and luteal interference in the toxic effects of Aroclor 1254 and against uterine tissue. (4) the first time in the vas deferens sperm abnormal sperm ratio, relative density, sperm motility, abnormal sperm rate and acrosome different periods of ontogeny came into contact with different doses of Aroclor 1254 the mouse spermatogenesis toxic quantitative. Prove the toxicity of Aroclor 1254 on spermatogenesis obvious dose-response relationship exists and the effect of the characteristics associated with ontogenetic stage. (5) the first time in the different periods of ontogeny contact AroCI sting 1254 male mice testis attached Chui histopathological findings on the mechanism of toxicity of spermatogenesis qualitative. Proof of abnormal sperm density, viability and morphology corresponding pathological changes of which the gonadal organs. (6) after the first demonstration contact Arodor 1254 male mice with normal female mice breeding, fertilization rate and the fertilized egg first cleavage rate significantly decreased, normal embryonic development rate decreased significantly. (7) to prove different the developmental stages contact AroClor1254 mice, histopathological changes in the internal organs, and existence of a dose-effect variation and developmental stages - the effect of changes in the characteristics.

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CLC: > Agricultural Sciences > Livestock, animal medicine,hunting,silkworm,bee > Animal Medicine ( Veterinary Medicine) > Veterinary Pharmacology > Veterinary Toxicology
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