Mechanism of action of endosulfan as disruptor of gonadal steroidogenesis in the cichlid fish Cichlasoma dimerus (original) (raw)
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Aquatic Toxicology, 2013
Endosulfan (ES), a persistent organochlorine pesticide, is widely used despite its toxicity to non-target animals. Upon reaching water bodies, ES can cause negative effects on aquatic animals, including disruption of hormonal systems. However, the action of ES on fish reproductive axis has been hardly studied thus far. The aim of the present work was to assess the endocrine disruptive potential of endosulfan on the pituitary gonadotropins levels and on the testes function due to ES in the South American freshwater fish Cichlasoma dimerus, using in vitro and in vivo approaches. In vitro experiments showed that ES inhibited the LH-stimulated steroidogenesis in gonads; no change was observed in gonadotropins release from pituitaries in culture. Laboratory waterborne ES (0.1, 0.3 and 1 g/L) exposure for two months caused decrease in FSH pituitary content and ␥GT activity in the testes (Sertoli cell function marker). Testicular histology revealed pathologies such as scarce intermediate stages of spermatogenesis, release of immature germ cells into the lobular lumen, presence of foam cells and interstitial fibrosis. As FSH and FSH-mediated steroidogenesis regulate spermatogenesis and Sertoli cell function, the effect of ES on FSH could be responsible for the morphological alterations observed in testes. In vitro, ES disrupted steroidogenesis in gonads, therefore similar effects in vivo cannot be ruled out. Based on this evidence, ES exhibits an endocrine disruptive action on the reproductive axis of C. dimerus, causing disruption at the pituitary and/or at the gonad level. These effects could acquire ecological significance under prolonged exposure to the pesticide in nature.
Archives of Environmental Contamination and Toxicology, 2010
Endocrine-disrupting chemicals can influence the hypothalamus-pituitary-gonad axis and possibly affect reproduction in vertebrates. We analyzed the effect of 30day endosulfan (ES) exposure in sexually undifferentiated larvae of the cichlid fish Cichlasoma dimerus. The number, area, mean cytoplasmic and nuclear diameter, and mean cytoplasmic optical density of gonadotropin-releasing hormone (GnRH) I, II, and III immunoreactive (ir-) neurons and b follicle-stimulating hormone (bFSH) ir-cells were measured. Animals exposed to the highest ES concentration (0.1 lg/l) showed a decrease in GnRH I nucleus/cytoplasm area ratio upon exposure. Nuclear area and mean nuclear diameter of bFSH ir-cells was higher in ES treated fish. bFSH nucleus/cytoplasm area ratio was high in exposed animals, and animals exposed to 0.1 lg/l ES showed smaller mean cytoplasmic optical density. These findings suggest that ES affects GnRH I and bFSH protein synthesis/release. However, these responses seem to be insufficient to affect gonadal differentiation at this stage of development.
Ecotoxicology and Environmental Safety, 2015
Endosulfan (ES) is an organochlorine pesticide widely used in agriculture despite its high toxicity towards non-target organisms such as fish. It has been demonstrated that ES can cause negative effects on aquatic animals, including disruption of hormonal systems. However, the alterations produced by this pesticide on the reproductive axis of fish prior to sexual maturity, as well as possible modes of action have hardly been studied. This study aimed at assessing the effect of waterborne exposure to the pesticide ES on the reproductive axis during sexual differentiation of juveniles of the South American freshwater cichlid fish Cichlasoma dimerus. No mortality was observed due to ES subchronic exposure (90 days post-fertilization). Exposure to ES did not affect body weight nor morphometric parameters, indicating that larvae nutritional state was not affected. Timing of sexual differentiation, gonadal morphology and sex ratio were likewise not altered by ES. However, ES acted as an endocrine disrupting chemical in this species as the morphometry of gonadotropin-releasing hormones (GnRH) producing cells was altered. Exposure to ES altered nuclear area, cell area and nucleus/cytoplasm ratio of GnRH II neurons, and cell and nuclear area and diameter of GnRH III neurons. Interestingly, in our previous study, exposure before sex differentiation (30 day exposure) caused no alteration to GnRH II and III, and did alter GnRH I and FSH cells. These alterations could lead to changes in circulating hormone levels, especially when fish are exposed for prolonged periods, ultimately impairing reproductive fitness. C. dimerus juveniles can be an interesting biological model to perform toxicological studies with the intent to assess early disruption endpoints in the reproductive axis during development.
Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology, 2012
Ovarian aromatase Brain aromatase Catfish Endocrine disruption Endosulfan Flutamide Ovarian development Tph2 immunoreactivity Juvenile Catfish(es), Clarias batrachus of 50 days post hatch (dph) were exposed to endosulfan (2.5 parts per billion [ppb]) and flutamide (33 ppb), alone and in combination for 50 days to access their impact on ovarian development. The doses used in this study were nominal considering pervious reports. Sampling was done at 100 dph to perform histology and measurement of various transcripts, estradiol-17β and aromatase activity. In general, treatments enhanced expression of ovary-specific transcription factors, steroidogenic enzymes steroidogenic acute regulatory protein and aromatases while transcripts of tryptophan hydroxylase2 (tph2) and catfish gonadotropin-releasing hormone declined in the brain of all treated groups with maximum reduction in the endosulfan group. Significant reduction of tph2 immunoreactivity in the forebrain/telencephalon-preoptic area endorsed our results. Increased number of pre-vitellogenic and less immature oocytes in the treated groups indicated hastened ovarian growth. Elevated ovarian aromatase activity and plasma estradiol-17β levels were noticed in the treated groups with maximum being in the endosulfan group. These data together demonstrate that the exposure of endosulfan causes synchronous precocious ovarian development better than flutamide, alone or in combination. Our results suggest that both endosulfan and flutamide alter ovarian growth by triggering precocious development in catfish.
Endosulfan and flutamide, a widely used pesticide and a prostate cancer/infertility drug, respectively, have an increased risk of causing endocrine disruption if they reach water bodies. Though many studies are available on neurotoxicity/bioaccumulation of endosulfan and receptor antagonism of flutamide, only little is known about their impact on testicular steroidogenesis at molecular level. Sex steroids play an important role in sex differentiation of lower vertebrates including fishes. Hence, a small change in their levels caused by endocrine disruptors affects the gonadal development of aquatic vertebrates significantly. The aim of this study was to evaluate the effects of endosulfan and flutamide on testisrelated transcription factor and steroidogenic enzyme genes with a comparison on the levels of androgens during critical period of catfish testicular development. We also analyzed the correlation between the above-mentioned genes and catfish gonadotropin-releasing hormone (cfGnRH)-tryptophan hydroxy-lase2 (tph2). The Asian catfish, Clarias batrachus males at 50 days post hatch (dph) were exposed to very low dose of endosulfan (2.5 g/L) and flutamide (33 g/L), alone and in combination for 50 days. The doses used in this study were far less than those used in the previous studies of flutamide and reported levels of endosulfan in surface water and sediments. Sampling was done at end of the treatments (100 dph) to perform testicular germ cell count (histology), measurements of testosterone (T) and 11-ketotestosterone (11-KT) by enzyme immunoassay and transcript quantification by quantitative real-time PCR. In general, treatments decreased the expression of several genes including testis-related transcription factors (dmrt1, sox9a and wt1), steroidogenic enzymes (11-hsd2, 17-hsd12 and P450c17), steroidogenic acute regulatory protein and orphan nuclear receptors (nr2c1 and Ad4BP/SF-1). In contrast, the transcripts of cfGnRH and tph2 were elevated in the brain of all treated groups with maximum elevation in the endosulfan group. However, combination of endosulfan and flutamide (E + F) treatment showed minor antagonism in a few results of transcript quantification. Levels of T and 11-KT were elevated after flutamide and E + F treatments while no change was seen in the endosulfan group signifying the effect of flutamide as an androgen receptor antagonist. All the treatments modulated testis growth by decreasing the progression of differentiation of spermatogonia to spermatocytes. Based on these results, we suggest that the exposure to endosulfan and flutamide, even at low doses, impairs testicular development either directly or indirectly at the level of brain.
Endosulfan is toxic to the reproductive health of male freshwater fish, Cyprinion watsoni
Die Naturwissenschaften, 2017
Endosulfan is an organochlorine pesticide that is toxic to aquatic life. Endosulfan might hamper the reproductive health of indigenous fish in agricultural areas of Pakistan where this pesticide is sprayed widely. The aim of the current study is to investigate the toxic effects of endosulfan on selected reproductive parameters of male freshwater fish, Cyprinion watsoni. Two concentrations of endosulfan (0.5 and 1 ppb for 30 days exposure) were tested for their effects on body weight, body length, and testicular weight, length, and width. Testicular testosterone was assayed from tissue extracts using enzyme immunoassay (EIA). A significant increase in the mortality rate was observed in both treated groups during both spawning and quiescent seasons. The overall behavior of fish in the aquarium was normal in all control and treated groups. However, the treated fish exhibited anxiety after treatment with endosulfan. The body weight and length, and testicular weight, length and width wer...
Risks Induced by Pesticides on Fish Reproduction
Pollution of water resources with agricultural water drainage has a great risk on fish reproduction. Organophosphrous pesticides such as Malathion and dimethaote are frequently used in Egypt due to their highly effectiveness for controlling agriculture pests. These pesticides were found that have endocrine disrupting effect on fish reproduction through lowering sex steroid hormones (estradiol and testosterone). Endocrine disrupting pesticides also have been implicated in the impairment of fish fecundity, semen quality, hatchability and survivability of fishes. Sex steroid hormones, vitellogenin, organosomatic indices and histopathology are considered as biomarker tools used for assessing disrupting effect of pesticides on fish.
Acta Scientific Veterinary Sciences, 2022
Endocrine disrupting chemicals (EDCs) are naturally occurring or synthetic molecules present in an ecosystem that have the potential to alter the production, release, transport, metabolism, binding, action, or elimination of natural hormones in the body. They act by mimicking endogenous hormones, antagonizing normal hormones, altering the natural pattern of hormone synthesis or metabolism, or modifying hormone receptors. The chemicals, particularly disrupting the reproductive system, can be androgenic, anti-androgenic, estrogenic or anti-estrogenic. This review provides a brief overview on spermatogenesis, disruption of spermatogenesis and effects of various EDCs on hormones involved in spermatogenesis. EDCs affect spermatogenesis in two ways, by affecting the development and function of male gonads or by disrupting the synthesis and action of hormones involved in spermatogenesis, such as, GnRH, gonadotropin, dihydroandrogen, 11-ketotestosterone, estrogen, and progesterone.
Environmental Biology of Fishes, 1993
Anabas testudineus were treated with non lethal levels of metacid-50 (0.106 ppb) and carbaryl(1.66 ppm) for 90 days covering the pre-spawning and spawning phases of the annual reproductive cycle. The main purpose of the present work was to identify the effects of metacid-50 and carbaryl on the gonado somatic index (GSI) and ovarian and plasma estrogen level. There was no alteration in GSI until 15 days, initiating the inhibition on day 20 which further intensified from 20 to 90 days of exposure. Plasma and ovarian estrogen level significantly increased up to 15 days of exposure followed by a decline till the end of the experiment. It is noteworthy that the effect of pesticides on GSI is reflected in the ovarian estrogen level. This highlights the fact that at short-term exposures the nonlethal levels of pesticides have no inhibitory effect while at long-term exposure, the pesticides have potent inhibitory effect on the reproduction of fish.