Acute Testicular Toxicity of 1,3-Dinitrobenzene and Ethylene Glycol Monomethyl Ether in the Rat: Evaluation of Biochemical Effect Markers and Hormonal Responses

Reader, S. C. J.; Shingles, C.; Stonard, Michael D.

doi:10.1093/toxsci/16.1.61

Cited by 7 publications

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“…Xenoestrogens like bisphenol A and methyl parathion have been reported to mediate reproductive toxicity by diminishing pituitary LH synthesis and secretion (Akingbemi et al, 2004;Maitra & Mitra, 2008). Our data are in agreement with previous studies on insecticide methomyl (Mahgoub & El-Medany, 2001), ethylene glycol monomethyl ether, a member of glycol ethers family (Reader et al, 1991) and bisphenol A (Atanassova et al, 2000). Kolaviron was previously reported to elicit protection against gonadotrophins suppression in di-n-butylphthalate-and cadmium-treated rats (Farombi et al, 2007;Farombi et al, 2012).…”

Section: Discussionsupporting

confidence: 92%

Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether-induced pituitary-thyroid axis toxicity in male rats

Adedara

Farombi

2012

Andrologia

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Endocrine disrupting chemicals cause reproductive dysfunction by interacting with intricate regulation and cellular processes involve in spermatogenesis. This study investigated the probable mechanism of action of ethylene glycol monoethyl ether (EGEE) as an antiandrogenic compound as well as the effects of kolaviron upon co-administration with EGEE in rats. Adult male rats were exposed to EGEE (200 mg kg(-1) bw) separately or in combination with either kolaviron [100 (KV1) and 200 (KV2) mg kg(-1) bw] or vitamin E (50 mg kg(-1) bw) for 14 days. Western blot analysis revealed that the administration of EGEE adversely affected steroidogenesis in experimental rats by decreasing the expression of steroid acute regulatory (StAR) protein and androgen-binding protein (ABP). EGEE significantly decreased the activities of 3β-hydroxysteroid dehydrogenase (3β-HSD) and 17β-hydroxysteroid dehydrogenase (17β-HSD) but markedly increased sialic acid concentration in rat testes. EGEE-treated rats showed significant decreases in plasma levels of luteinising hormone (31%), testosterone (57.1%), prolactin (80.9%), triiodothyronine (65.3%) and thyroxine (41.4%), whereas follicle-stimulating hormone was significantly elevated by 76.9% compared to the control. However, co-administration of kolaviron or vitamin E significantly reversed the EGEE-induced steroidogenic dysfunction in rats. This study suggests that kolaviron may prove promising as a chemoprotective agent against endocrine pathology resulting from EGEE exposure.

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Section: Discussionsupporting

confidence: 92%

Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether-induced pituitary-thyroid axis toxicity in male rats

Adedara

Farombi

2012

Andrologia

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“…The ABP produced by SCs has also been proposed as a biomarker of the normal occurrence of spermatogenesis (Rehnberg et al ., ). However, plasma concentration of ABP is not always directly associated with the concentrations detected in the testis and interstitial fluid (Reader et al ., ; Rehnberg et al ., ). Finally, the metabolic cooperation established between SC–germ cells has also been shown to serve as an indicator for the success of spermatogenesis.…”

Section: Discussionmentioning

confidence: 97%

Sertoli cell as a model in male reproductive toxicology: Advantages and disadvantages

Reis

Moreira

Sousa

et al. 2015

J of Applied Toxicology

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Pressure towards population aging in the demographic pyramid is not only due to sociological/personal choices but also due to subfertility or infertility. There are several chemicals and mixtures that impair male fertility. While experimental animal models are crucial to identify compounds that affect male fertility, it is essential to use reliable in vitro models to determine cellular targets and intracellular pathways that mediate chemical toxicity in the male reproductive system. In this review, we focused on the somatic Sertoli cell (SC) that, within the testis, is a major target for hormonal signaling and provides physical and nutritional support to developing germ cells. The different outcomes possible in each type of study: in vivo versus in vitro (either in primary or immortalized cell cultures) are analyzed. Herein, we intend to clarify the unique features that render SCs as excellent candidates for a robust in vitro model to study the deleterious effects of chemicals on male reproductive health. The sensitivity of SCs to toxicants/pharmaceuticals is discussed and, based on the literature reviewed we propose the in vitro study of SC physiology as a model to disclose deleterious effects of substances to male fertility.

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“…[18], którzy zaobserwowali spadek stężenia testosteronu w jądrach i jego wzrost w surowicy, podwyższony poziom folitropiny (follicle-stimulating hormone -FSH) w surowicy oraz wzrost poziomu białka wiążącego androgeny (androgen binding protein -ABP) w surowicy szczurów otrzymujących EGME per os w dawkach jednorazowych 100--500 mg/kg m.c. Zmiany histopatologiczne w jądrach w postaci znacznego ubytku spermatocytów i spermatyd, występujące po 16 godz.…”

Section: Wyniki Przegląduunclassified

Ethylene glycol and propylene glycol ethers – Reproductive and developmental toxicity

Starek‐Świechowicz

Stárek

2015

Med Pr

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StreszczenieEtery alkilowe glikolu etylenowego (ethylene glycol alkyl ethers -EGAE) i propylenowego (propylene glycol alkyl ethers -PGAE) są szeroko stosowane w przemyśle i gospodarstwie domowym, głównie jako rozpuszczalniki. Niektóre EGAE wykazują działanie gonadotoksyczne, embriotoksyczne, fetotoksyczne i teratogenne zarówno u ludzi, jak i zwierząt doświadczalnych. Ze względu na szkodliwe działanie tych eterów na rozrodczość i rozwój organizmu EGAE są zastępowane znacznie mniej toksycznymi PGAE. W niniejszej pracy przedstawiono dane na temat mechanizmów toksycznego działania EGAE na komórki rozrodcze, zarodek i płód. Szczególną uwagę zwrócono na metabolizm niektórych EGAEs i ich toksyczność narządową, a także na apoptozę spermatocytów związaną ze zmianami ekspresji genów, które kodują czynniki stresu oksydacyjnego, kinazy białkowe i jądrowe receptory hormonów. Med. Pr. 2015;66(5):725-737Słowa kluczowe: etery glikolu etylenowego, etery glikolu propylenowego, toksyczność rozwojowa, mechanizmy toksyczności, toksyczność reprodukcyjna, apoptoza AbstractBoth ethylene and propylene glycol alkyl ethers (EGAEs and PGAEs, respectively) are widely used, mainly as solvents, in industrial and household products. Some EGAEs demonstrate gonadotoxic, embriotoxic, fetotoxic and teratogenic effects in both humans and experimental animals. Due to the noxious impact of these ethers on reproduction and development of organisms EGAEs are replaced for considerably less toxic PGAEs. The data on the mechanisms of testicular, embriotoxic, fetotoxic and teratogenic effects of EGAEs are presented in this paper. Our particular attention was focused on the metabolism of some EGAEs and their organ-specific toxicities, apoptosis of spermatocytes associated with changes in the expression of various genes that code for oxidative stress factors, protein kinases and nuclear hormone receptors. WSTĘPEtery alkilowe glikolu etylenowego (ethylene glycol alkyl ethers -EGAE) i propylenowego (propylene glycol alkyl ethers -PGAE) są produktami addycji odpowiednio tlenku etylenu i tlenku propylenu z pierwszorzędo-wymi alkoholami alifatycznymi. Reakcje te przebiegają w warunkach podwyższonego ciśnienia i temperatury oraz w obecności katalizatora. Ponieważ w tych reakcjach dochodzi także do procesu poliaddycji tlenków alkilowych, oprócz eterów monoetylenowych i monopropylenowych powstają również odpowiednie dii trietery o większych masach cząsteczkowych i mniejszej lotności od monomerów. Związki te umownie nazwano eterami serii E i serii P [1].Do eterów glikolowych serii E należą m.in.: n metoksyetanol (ethylene glycol methyl ether -EGME) (numer CAS: 109-86-4), n etoksyetanol (ethylene glycol ethyl ether -EGEE) (110-80-5), n butoksyetanol (ethylene glycol butyl ether -EGBE) (111-76-2), n metoksydietanol (diethylene glycol methyl ether -DEGME) (111-77-3), n etoksydietanol (diethylene glycol ethyl ether -DEGEE) (111-90-0),

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Acute Testicular Toxicity of 1,3-Dinitrobenzene and Ethylene Glycol Monomethyl Ether in the Rat: Evaluation of Biochemical Effect Markers and Hormonal Responses

Cited by 7 publications

References 0 publications

Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether-induced pituitary-thyroid axis toxicity in male rats

Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether-induced pituitary-thyroid axis toxicity in male rats

Sertoli cell as a model in male reproductive toxicology: Advantages and disadvantages

Ethylene glycol and propylene glycol ethers – Reproductive and developmental toxicity

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