Gender-Specific Adverse Effects of Mono-Ethylhexyl Phthalate on Steroidogenesis in Immature Granulosa Cells and Rat Leydig cell Progenitors in vitro

Svechnikova, Konstantin; Svechnikova, Irina; Söder, Olle

doi:10.3389/fendo.2011.00009

Cited by 14 publications

(13 citation statements)

References 35 publications

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“…Further, MEHP exposure for 24 h at 100 μM decreased progesterone production and FSH-induced cAMP accumulation in rat granulosa cells ( 164 ). In contrast, MEHP exposure for 48 h at 100–250 μM in a different study increased basal steroidogenesis in rat granulosa cells, evident by increases in progesterone and protein levels of STAR ( 165 ). Perhaps the discrepancy in the MEHP-induced defects in steroidogenesis can be attributed to the dosage and use of different rat strains and the different susceptibilities to phthalate toxicity across strains.…”

Section: Effects Of Phthalates On Steroidogenesismentioning

confidence: 82%

The Effects of Phthalates on the Ovary

2015

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Phthalates are commonly used as plasticizers in the manufacturing of flexible polyvinyl chloride products. Large production volumes of phthalates and their widespread use in common consumer, medical, building, and personal care products lead to ubiquitous human exposure via oral ingestion, inhalation, and dermal contact. Recently, several phthalates have been classified as reproductive toxicants and endocrine-disrupting chemicals based on their ability to interfere with normal reproductive function and hormone signaling. Therefore, exposure to phthalates represents a public health concern. Currently, the effects of phthalates on male reproduction are better understood than the effects on female reproduction. This is of concern because women are often exposed to higher levels of phthalates than men through their extensive use of personal care and cosmetic products. In the female, a primary regulator of reproductive and endocrine function is the ovary. Specifically, the ovary is responsible for folliculogenesis, the proper maturation of gametes for fertilization, and steroidogenesis, and the synthesis of necessary sex steroid hormones. Any defect in the regulation of these processes can cause complications for reproductive and non-reproductive health. For instance, phthalate-induced defects in folliculogenesis and steroidogenesis can cause infertility, premature ovarian failure, and non-reproductive disorders. Presently, there is a paucity of knowledge on the effects of phthalates on normal ovarian function; however, recent work has established the ovary as a target of phthalate toxicity. This review summarizes what is currently known about the effects of phthalates on the ovary and the mechanisms by which phthalates exert ovarian toxicity, with a particular focus on the effects on folliculogenesis and steroidogenesis. Further, this review outlines future directions, including the necessity of examining the effects of phthalates at doses that mimic human exposure.

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Section: Effects Of Phthalates On Steroidogenesismentioning

confidence: 82%

The Effects of Phthalates on the Ovary

2015

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“…It was found to decrease viability as well as steroidogenic potential of mouse Leydig tumor cells (Piché et al, ). This phthalate stimulated basal steroidogenesis and steroidogenic acute regulatory protein (StAR) expression in both types of steroidogenic cells (Svechnikova, Svechnikova, & Söder, ).…”

Section: Introductionmentioning

confidence: 99%

Effect of mono‐(2‐ethylhexyl) phthalate (MEHP) on proliferation of and steroid hormone synthesis in rat ovarian granulosa cells in vitro

Liu

Guo

et al. 2017

Journal Cellular Physiology

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This study aimed to examine the proliferation of and secretion by rat ovarian granulosa cells (GCs) treated with mono-(2-ethylhexyl) phthalate (MEHP). Ovarian GCs were incubated with MEHP at concentration of 0, 25, 50, 100, and 200 µM for 24 hr. Cell viability was determined using the MTT Cell Proliferation Assay. Progesterone and estradiol production was evaluated by radioimmunoassay (RIA) and the expression of FSHR, PR, and ER was measured by immunocytochemistry. StAR, P450scc, 3β-HSD, 17β-HSD, and P arom mRNA levels were determined by RT-PCR. MEHP markedly attenuated proliferation of GCs, increased expression of sex hormone receptors and key enzymes in progesterone production, and stimulated steroid hormone secretion. The result of these analyses demonstrates that MEHP exposure of GCs may have effects on rat ovarian functions.

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“…In addition to acrosome biogenesis defects, we observed a decrease in sperm count; this appears to be a common phenotype for a variety of genetic defects that perturb the normal programme of mouse spermiogenesis (Kang-Decker et al, 2001;Venables and Cooke, 2000;Wang et al, 2014). Bell et al (2014) found that the histone to protamine transition was disrupted in Sirt1-deficient spermatids, and this might partially account for the decrease in sperm count.…”

Section: Discussionmentioning

confidence: 68%

“…Leydig cells were isolated as previously described, with minor modifications (Svechnikova et al, 2011). Briefly, the 2-month-old mice were euthanized by cervical dislocation, and the testes were removed and washed three times with PBS.…”

Section: Isolation and Primary Culture Of Leydig Cellsmentioning

confidence: 99%

Sirt1 regulates acrosome biogenesis by modulating autophagic flux during spermiogenesis in mice

Liu¹,

Song²,

Wang³

et al. 2017

Journal of Cell Science

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Sirt1 is a member of the sirtuin family of proteins and has important roles in numerous biological processes. Sirt1 −/− mice display an increased frequency of abnormal spermatozoa, but the mechanism of Sirt1 in spermiogenesis remains largely unknown. Here, we report that Sirt1 might be directly involved in spermiogenesis in germ cells but not in steroidogenic cells. Germ cell-specific Sirt1 knockout mice were almost completely infertile; the early mitotic and meiotic progression of germ cells in spermatogenesis were not obviously affected after Sirt1 depletion, but subsequent spermiogenesis was disrupted by a defect in acrosome biogenesis, which resulted in a phenotype similar to that observed in human globozoospermia. In addition, LC3 and Atg7 deacetylation was disrupted in spermatids after knocking out Sirt1, which affected the redistribution of LC3 from the nucleus to the cytoplasm and the activation of autophagy. Furthermore, Sirt1 depletion resulted in the failure of LC3 to be recruited to Golgi apparatus-derived vesicles and in the failure of GOPC and PICK1 to be recruited to nucleus-associated acrosomal vesicles. Taken together, these findings reveal that Sirt1 has a novel physiological function in acrosome biogenesis.

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Gender-Specific Adverse Effects of Mono-Ethylhexyl Phthalate on Steroidogenesis in Immature Granulosa Cells and Rat Leydig cell Progenitors in vitro

Cited by 14 publications

References 35 publications

The Effects of Phthalates on the Ovary

The Effects of Phthalates on the Ovary

Effect of mono‐(2‐ethylhexyl) phthalate (MEHP) on proliferation of and steroid hormone synthesis in rat ovarian granulosa cells in vitro

Sirt1 regulates acrosome biogenesis by modulating autophagic flux during spermiogenesis in mice

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