Effects of arsenic exposure during the pre- and postnatal development on the puberty of female offspring (original) (raw)
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Adverseeffectsofarsenicexposureonuterinefunctionandstructurein female rat
The present investigation examined the adverse effects of arsenic exposure on uterine function and structure of female rat at 56 days of age, exposed to different doses (50, 100, and 200 ppm) of sodium arsenite in drinking water at immature age (28 days) for 28 days. Dose-dependent decrease (Po0.001) was observed in mean uterine weight and length in all treated groups compared to control. Higher arsenic deposition was found in uterine tissue against increased doses of arsenite. Arsenite treatment altered the histomormphology of the uterus. Uterine epithelium in 50 ppm group was lined by cuboidal cells instead of columnar cells observed in control epithelium. In 100 and 200 ppm groups, no demarcation was observed between epithelial cells and endometrial stroma. No basement membrane was seen in these groups; even in 50 ppm, basement membrane was disturbed. The endometrial stroma in 100 and 200 ppm groups was very dense in appearance and contained irregular-shaped cells. In myometrium, loosening of cells was observed in 100 and 200 ppm groups. Dose-dependent decrease (Po0.001) was observed in mean uterine diameter, epithelial height, thickness of endometrium, myometrium, and in plasma levels of estradiol, progesterone, FSH and LH in all the treatment groups compared to control. In summary, arsenic is a major threat to female reproductive health acting as a reproductive toxicant and as an endocrine disruptor, restricted the function and structure of uterus, by altering the gonadotrophins and steroid levels, not only at high dose concentration but also at low (50 ppm) levels, when they become mature.
A study on the effects of arsenic toxicity on oviduct histomorphology in the female rat
Journal of Histotechnology, 2018
Arsenic-contaminated drinking water and its association to different diseases has been considered a severe problem worldwide. The goal of the present study was to evaluate the histopathological changes in oviduct of female rat following 4-week exposure to different doses (50, 100, and 200 ppm) of sodium arsenite. Treatment was initiated when rat reaches the age of 4 weeks. Body weight of animals was recorded weekly. Weight, diameter, and arsenic deposition in oviduct were estimated. Based on anatomical division of oviduct, histology of isthmus and ampulla was examined for any histopathological changes. A dose-dependent decrease was observed in body weight and oviduct weight of treated rats as compared to untreated control rat and low-dose group. Higher arsenic deposition was found in oviduct with the increased doses of arsenite. Cellular arrangement was found disorganized and loosely packed in the epithelium and muscle layers of all treated groups, but was more conspicuous at 200 ppm dosage. Fewer cilia were seen in isthmus and ampulla of treated groups, and almost no cilia were observed in isthmus of 200 ppm group. Muscle layer thickness and epithelium height of arsenic treated rats was reduced in a dose-dependent manner from low (50 ppm) to high group (200 ppm) as compared to control rats. This study found that arsenite treatment adversely affected the body weight of female rats and induced histopathological changes in the cellular structure, configuration, and organization of oviduct in female rats.
The present study aimed to assess the possible interference of sodium arsenite in F1 generation male mice with special reference to steroidogenic marker enzymes. Mice were devided in to two groups. The mice in first were served as control and recived normal tap water. Sodium arsenite administered orally to mice in the second group during pregnancy and lactation at a dose level of 0.4 ppm and analyzed for spermatogenesis and steroidogenesis in next generation adult male mice. The activity levels of selected steroidogenic marker enzymes (3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase) decreased significantly in mice exposed to sodium arsenite. The circulatory levels of testosterone decreased significantly in experimental mice with an increase in follicle stimulating hormone. The decreased levels of testosterone with elevated follicle stimulating hormone and lutenizing hormone levels in mice exposed to arsenic during early stages of development are indicative of intact pituitary-testicular axis. The results indicate that exposure to arsenic during early stages of development suppresses the male reproduction in adults. Thus, we conclude that the potential of reproduction is programmed, to some extent, in the early stages of development and hence any toxic insult during embryonic development and lactation suppresses male reproductive potential in adulthood.
The present study aimed to assess the possible interference of sodium arsenite in F1 generation male mice with special reference to steroidogenic marker enzymes. Mice were divided in to two groups. The mice in first were served as control and received normal tap water. Sodium arsenite administered orally to mice in the second group during pregnancy and lactation at a dose level of 0.4 ppm and analyzed for spermatogenesis and steroidogenesis in next generation adult male mice. The activity levels of selected steroidogenic marker enzymes (3-hydroxysteroid dehydrogenase and 17-hydroxysteroid dehydrogenase) decreased significantly in mice exposed to sodium arsenite. The circulatory levels of testosterone decreased in experimental mice with significantly increase in follicle stimulating hormone. The decreased levels of testosterone with elevated follicle stimulating hormone and luteinizing hormone levels in mice exposed to arsenic during early stages of development are indicative of intact pituitary-testicular axis. The results indicate that exposure to arsenic during early stages of development suppresses the male reproduction in adults. Thus, we conclude that the potential of reproduction is programmed, to some extent, in the early stages of development and hence any toxic insult during embryonic development and lactation suppresses male reproductive potential in adulthood.
Reproductive Toxicology, 2014
Arsenic (As) is a prevalent environmental toxin; readily accessible for human consumption and has been identified as an endocrine disruptor. However, it is not known what impact As has on female sexual maturation. Therefore, in the present study, we investigated the effects of prepubertal exposure on mammary gland development and pubertal onset in female rats. Results showed that prepubertal exposure to 10mg/kg of arsenite (As(III)) delayed vaginal opening (VO) and prepubertal mammary gland maturation. We determined that As accumulates in the liver, disrupts hepatocyte function and suppresses serum levels of the puberty related hormone insulinlike growth factor 1 (IGF-1) in prepubertal animals. Overall, this is the first study to show that prepubertal exposure to As(III) acts peripherally to suppresses circulating levels of IGF-1 resulting in delayed sexual maturation. Furthermore, this study identifies a critical window of increased susceptibility to As(III) that may have a lasting impact on female reproductive function.
The Effects of Maternal Exposure Riboflavin to Prevent Uterus Arsenic Damage in Offspring Rats
Journal of Human Environment and Health Promotion, 2021
Background: In this study, the efficacy of riboflavin (VB2) in preventing uterus As2O3 damage was investigated for the first time in the literature. Methods: The rats received 40 μg LHRHa for estrus synchronization. 48 pregnant Wistar rats were included in the study. Four groups were formed with 7 rats in each group: Sham, 1.5 mg arsenic trioxide (As2O3/L) alone or in combination with VB2 (20 and 40 mg/L) in drinking water (for 21 days continuously). Moreover, similar to maternal generation treatment the F1-female generation was arranged (for 35 days continuously until puberty). Results: Based on the results, As2O3 reduced body weight and feed intake (P < 0.05). Furthermore, the serum malondialdehyde levels in the As2O3 group were significantly higher than that of the control group (P < 0.05). At the same time, the total antioxidative status and the activities of glutathione peroxidase, superoxide dismutase, and catalase were reduced (P < 0.05). Meanwhile, As2O3 remarkably increased the inflammatory markers production [interleukin 6 and C-reactive protein] (P < 0.05). As2O3 administration induced uterus apoptosis-related genes by upregulating caspase-3, iNOS, and Bax genes and downregulating Bcl-2 gene of pubertal F1-female rats (P < 0.05). Conclusion: Our observation indicated that VB2 therapy is potentially an effective strategy to modify the detrimental effects of As2O3 in pubertal F1-female rats via suppresses oxidative damages.
Effect of Transplacental and Lactational Exposure to Arsenic on Male Reproduction in Mice
… of Reproduction and …, 2011
Sodium arsenite was orally administered to mice during pregnancy and lactation at a dose level of 0.4 ppm and spermatogenesis of next generation in adult male mice was analyzed. A significant depletion in sperm count, sperm motility, sperm viability and HOS-coiling was observed in mice exposed to arsenic during early stages of development with an increase in sperm abnormalities. These results indicated that exposure to arsenic during early stages of development suppresses the male reproduction in adults. Thus, it was concluded that the potential of reproduction is programmed, to some extent, in the early stages of development and hence any toxic insult during embryonic development and lactation suppresses male reproductive potential in adulthood.
Fertility in male rats: Disentangling adverse effects of arsenic compounds
Reproductive toxicology (Elmsford, N.Y.), 2018
Arsenic impairs male reproductive functions. However, it is not clear whether different arsenic compounds similarly affect fertility. In this study, we compared the impact of sodium arsenite and arsenate on sperm quality and fertility. After 56 d exposure, male Wistar rats were mated and pregnant females were evaluated by fertility indexes. Clearly, exposure to 10 mg/L arsenite reduced daily sperm production via HO overproduction and germ cells loss. Animals from this group also showed a decrease in epididymal sperm counts and percentage of sperm with intact membranes. Moreover, they presented low fertility potential and high preimplantation loss. In contrast, 10 mg/L arsenate caused oxidative stress in testis, mineral imbalance in epididymis, and sperm membranes damage, with no effects on fertility. Both arsenic compounds at 0.01 mg/L altered reproductive parameters. We concluded that arsenite is more harmful than arsenate to sperm quality and male fertility, with negative influenc...
2012
3 Abstract: Sodium arsenite was orally administered to mice during pregnancy and lactation at a dose level of 0.4 ppm and body weights and organ weights with special focus to reproductive organs in next generation adult male mice were analyzed. The body weight and weight gain of control and experimental pups did not differ significantly. However, the weights of testes, prostate and seminal vesicle decreased in experimental mice when compared with controls. Histology of testes indicated decrease in primary and secondary spermatocytes and spermatids in experimental mice when compared with control. These results indicated that exposure to arsenic during early stages of development suppresses the development of male reproductive organs in adults. Thus, it was conclude that the potential of reproduction is programmed, to some extent, in the early stages of development and hence any toxic insult during embryonic development and lactation suppresses male reproductive potential in adulthood.
Arsenic abrogates the estrogen-signaling pathway in the rat uterus
Reproductive Biology and Endocrinology, 2010
Background: Arsenic, a major pollutant of water as well as soil, is a known endocrine disruptor, and shows adverse effects on the female reproductive physiology. However, the exact molecular events leading to reproductive dysfunctions as a result of arsenic exposure are yet to be ascertained. This report evaluates the effect and mode of action of chronic oral arsenic exposure on the uterine physiology of mature female albino rats. Methods: The effect of chronic oral exposure to arsenic at the dose of 4 microg/ml for 28 days was evaluated on adult female albino rats. Hematoxylin-eosin double staining method evaluated the changes in the histological architecture of the uterus. Circulating levels of gonadotropins and estradiol were assayed by enzyme-linked immunosorbent assay. Expression of the estrogen receptor and estrogen-induced genes was studied at the mRNA level by RT-PCR and at the protein level by immunohistochemistry and western blot analysis. Results: Sodium arsenite treatment decreased circulating levels of estradiol in a dose and time-dependent manner, along with decrease in the levels of both LH and FSH. Histological evaluation revealed degeneration of luminal epithelial cells and endometrial glands in response to arsenic treatment, along with reduction in thickness of the longitudinal muscle layer. Concomitantly, downregulation of estrogen receptor (ER alpha), the estrogen-responsive gene-vascular endothelial growth factor (VEGF), and G1 cell cycle proteins, cyclin D1 and CDK4, was also observed. Conclusion: Together, the results indicate that arsenic disrupted the circulating levels of gonadotropins and estradiol, led to degeneration of luminal epithelial, stromal and myometrial cells of the rat uterus and downregulated the downstream components of the estrogen signaling pathway. Since development and functional maintenance of the uterus is under the influence of estradiol, arsenic-induced structural degeneration may be attributed to the reduction in circulating estradiol levels. Downregulation of the estrogen receptor and estrogen-responsive genes in response to arsenic indicates a mechanism of suppression of female reproductive functions by an environmental toxicant that is contra-mechanistic to that of estrogen.