2020
DOI: 10.1016/j.scitotenv.2020.140293
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Di-(2-ethylhexyl) phthalate induced developmental abnormalities of the ovary in quail (Coturnix japonica) via disruption of the hypothalamic-pituitary-ovarian axis

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Cited by 58 publications
(27 citation statements)
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“…Section of testis showed a complete absence of spermatids and stopping the spermatogenesis process; these results were found agreed with many articles that showed DEHP produced testicular toxicity and damages to tubules and spermatogenesis in all stages; also, DEHP induces vacuolar degeneration in Sertoli and Leydig cells (23). Section of quail's ovary showed complete absence of primordial follicles which consider the first step in developing follicles with hemorrhages, vacuolar degeneration in granular cell of interstitial tissue with infiltration of inflammatory cells, these result can be explained by the effect of MEHP the main metabolic of DEHP that cause decrease and stop estradiol production from ovary the activate peroxisomes receptors in the granulosa cells of developing follicles cause them to undergo apoptosis, all these outcomes suggest that the primary site of toxicity for DEHP is the granulosa cell of growing pre-ovulatory follicles which cause complete absent of these primordial follicles and lead to cystic ovary in cases where the exposure occur after puberty, on other hand the ovary from quails were they exposed to DEHP since one day old their ovary showed complete absent of growing and ovulatory follicles (24), the same results were have been recorded by other studies (25,26) in which the vacuolar degeneration in granular cell layer of ovary with hemorrhage are the most significant outcomes in DEHP toxicity in rats.…”
Section: Discussionsupporting
confidence: 77%
“…Section of testis showed a complete absence of spermatids and stopping the spermatogenesis process; these results were found agreed with many articles that showed DEHP produced testicular toxicity and damages to tubules and spermatogenesis in all stages; also, DEHP induces vacuolar degeneration in Sertoli and Leydig cells (23). Section of quail's ovary showed complete absence of primordial follicles which consider the first step in developing follicles with hemorrhages, vacuolar degeneration in granular cell of interstitial tissue with infiltration of inflammatory cells, these result can be explained by the effect of MEHP the main metabolic of DEHP that cause decrease and stop estradiol production from ovary the activate peroxisomes receptors in the granulosa cells of developing follicles cause them to undergo apoptosis, all these outcomes suggest that the primary site of toxicity for DEHP is the granulosa cell of growing pre-ovulatory follicles which cause complete absent of these primordial follicles and lead to cystic ovary in cases where the exposure occur after puberty, on other hand the ovary from quails were they exposed to DEHP since one day old their ovary showed complete absent of growing and ovulatory follicles (24), the same results were have been recorded by other studies (25,26) in which the vacuolar degeneration in granular cell layer of ovary with hemorrhage are the most significant outcomes in DEHP toxicity in rats.…”
Section: Discussionsupporting
confidence: 77%
“…42,43 ATZ, which is used widely in the agricultural sector, has been recognized as a toxic environmental pollutant for humans. 22 Previous studies have determined that ATZ exposure disturbs the splenic homeostasis by inducing the apoptosis of splenocytes. 21,28 Lyc prevented the damage of ATZ-induced in different tissues via mice and rats.…”
Section: Discussionmentioning
confidence: 99%
“…See DOI: 10.1039/d1fo02857j Some studies have found that ATZ could induce inflammation in some tissues. [22][23][24] In addition, ATZ exposure can result in ROS generation and accumulation in its target organs. Thus, it could be hypothesized that ATZ induced the activation of Nlrp3, which could trigger autoinflammatory and metabolic disorders in human.…”
Section: Introductionmentioning
confidence: 99%
“…It induced ovarian toxicity by inhibition of follicular development and abnormal steroid hormone synthesis in cultured rat ovarian follicles 85 . It also inhibited the rat granulosa cell viability, increased apoptosis through caspase‐3 activation and Bcl‐2‐associated x protein (BAX) expression, stimulated steroid hormone secretion, and induced the expression of key enzymes in progesterone expression and sex hormone receptors 86‐88 …”
Section: Effects Of Phthalate On Granulosa Cellsmentioning
confidence: 99%
“…Moreover, DEHP affected the anti‐apoptosis function of KIT ligand (KITL) and growth differentiation factor‐9 (GDF‐9) and increased the BAX/ BCL2 expression ratio to promote apoptosis of the granulosa cells 95 . Recently, Li et al 88 demonstrated that quails fed on DEHP showed mitochondrial damage and decreased thickness of the ovarian granulosa cell layer, along with oxidative stress.…”
Section: Effects Of Phthalate On Granulosa Cellsmentioning
confidence: 99%