Effect of aldrin on spermatogenesis, plasma gonadotrophins and testosterone, and testicular testosterone in the rat

Chatterjee, S.; Ray, Aritra; Ghosh, Surajit; Bhattacharya, Sayantani Sarkar; Pakrashi, Anita; Deb, Chandicharan

doi:10.1677/joe.0.1190075

Cited by 18 publications

(7 citation statements)

References 25 publications

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“…24,54 The exact mechanism through which quinalphos induces these alterations in testes is not clear. It has been reported that luteinizing hormone and folliclestimulating hormone, which are required to obtain nor-mal testicular function, are down-regulated in quinalphos-treated rats, 15,16,17,36 acting primarily at the level of the pituitary. 17 It has also been observed that an increase in testicular lipid peroxidation causes a decrease in the production of testicular androgen.…”

Section: Quinalphos-induced Destabilization Of Membrane Fluidity and mentioning

confidence: 99%

“…[4][5][6][7][8][9][10] Some of these pesticides have the ability to mimic the natural oestrogens, which are popularly known as xeno-oestrogens or environmental oestrogens, 10,11 and may have a damaging effect on the reproductive system and deleterious effects on the central nervous system function of both humans and wildlife. 4,10,[12][13][14][15][16] Earlier investigations revealed that different pesticides and insecticides, on their exposure to the reproductive system, cause varying degrees of testicular dysfunction and brain disorder in man and also in experimental animals. 13,15,16 Quinalphos (O,O-diethyl-O-[quinoxalinyl- (2)-thionophosphate]), one such environmental xeno-oestrogenic insecticide, is known to interfere with the expression of the sex hormones leading to abnormalities in both male and female reproductive organs in Wistar albino rats.…”

Section: Introductionmentioning

confidence: 99%

“…4,10,[12][13][14][15][16] Earlier investigations revealed that different pesticides and insecticides, on their exposure to the reproductive system, cause varying degrees of testicular dysfunction and brain disorder in man and also in experimental animals. 13,15,16 Quinalphos (O,O-diethyl-O-[quinoxalinyl- (2)-thionophosphate]), one such environmental xeno-oestrogenic insecticide, is known to interfere with the expression of the sex hormones leading to abnormalities in both male and female reproductive organs in Wistar albino rats. 4,15,17,18 Tissue degeneration is a free-radical-mediated process that involves lipid peroxides and lipid peroxidation of polyunsaturated fatty acids (PUFA) of the mammalian tissue.…”

Section: Introductionmentioning

confidence: 99%

“…13,15,16 Quinalphos (O,O-diethyl-O-[quinoxalinyl- (2)-thionophosphate]), one such environmental xeno-oestrogenic insecticide, is known to interfere with the expression of the sex hormones leading to abnormalities in both male and female reproductive organs in Wistar albino rats. 4,15,17,18 Tissue degeneration is a free-radical-mediated process that involves lipid peroxides and lipid peroxidation of polyunsaturated fatty acids (PUFA) of the mammalian tissue. [19][20][21][22][23][24] In a developing rat, brain quinalphos (QP) produces cerebral oxidative stress that enhances brain lipid peroxidation, which may be recovered after withdrawal of the drug.…”

Section: Introductionmentioning

confidence: 99%

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Study of quinalphos (an environmental oestrogenic insecticide) formulation (Ekalux 25 E.C.)-induced damage of the testicular tissues and antioxidant defence systems in Sprague-Dawley albino rats

Debnath

Mandal

2000

J. Appl. Toxicol.

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The effect of quinalphos (O-O-diethyl-O-[quinoxalinyl-(2)-thionophosphate]), an environmental oestrogenic organophosphorus insecticide pollutant, was studied on Sprague-Dawley albino rats at doses of 250 and 500 microgram kg(-1) body wt. i.p. for 3, 8 and 15 days, respectively. After the treatment with quinalphos there was an increase in the lipid peroxides (as measured by manoldialdehyde production) and a decrease in the total lipid content for the testicular membrane. The effects were more pronounced at the low doses than at the higher doses, indicating that some physiological defence mechanisms were in operation at higher doses. The free-radical-scavenging enzymes (superoxide dismutase, catalase and glutathione peroxidase) showed significantly higher activity at high dose in comparison to their activities at low-dose treatment. Glutathione content was gradually reduced after quinalphos treatment, both in low and high doses. Histomorphohological studies showed that after the low-dose treatment shrinkage of the tubular diameter and testicular atrophy leading to degenerative changes in the germinal epithelium were observed. But at high dose, gradual recovery of various germ cell layers and significant expansion of seminiferous tubules of Sprague-Dawley rat testes were found; the latter is generally believed to be a useful index of testicular activity through the hypothalamo-hypophyseal-gonadal axis. The present study indicates that quinalphos caused damage and degeneration of the testicular tissues due to free-radical-mediated lipid peroxidation at low doses. We have also demonstrated that, in response to the damage, an endogenous antioxidant enzyme defence system became operative at the higher dose of treatment.

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Section: Quinalphos-induced Destabilization Of Membrane Fluidity and mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Study of quinalphos (an environmental oestrogenic insecticide) formulation (Ekalux 25 E.C.)-induced damage of the testicular tissues and antioxidant defence systems in Sprague-Dawley albino rats

Debnath

Mandal

2000

J. Appl. Toxicol.

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“…Aldrin accumulates in the testis, although, to a lesser extent than in other tissues (66). Treatment of rats with aldrin inhibited intratesticular and circulating testosterone levels and affected spermatogenesis (67). Heptachlor is an insecticide used in the control of termites and in the cotton industry.…”

Section: Organochlorinesmentioning

confidence: 99%

Environmental Factors That Disrupt Leydig Cell Steroidogenesis

Papadopoulos

Contemporary Endocrinology

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Leydig cells of the testis are responsible for the biosynthesis and secretion of androgens, critical for developmental and reproductive function in the male. Disruption of testosterone biosynthesis by environmental factors can cause sexual dysfunction, infertility, or sterility. The present review focuses on the toxicological effects of agricultural and industrial chemicals on Leydig cell steroidogenesis. An evaluation of the molecular targets of the reviewed chemicals identifies three major sites of action mediating their toxic effects on Leydig cell steroidogenesis. These are the luteinizing hormone-induced signal transduction pathway, cholesterol transport into mitochondria, and steroidogenic enzyme activity and/or expression.

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Miscellaneous Chlorinated Hydrocarbon Pesticides

Bus¹,

Leber²

2001

Patty's Toxicology

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This chapter presents information on two structurally and toxicologically different classes of chlorinated pesticides: the organochlorine insecticides and the herbicide 2,4‐dichlorophenoxyacetic acid (2,4D). The first group described, the chlorinated hydrocarbon insecticides, belong to a structural class containing only carbon, hydrogen and chlorine. This pesticide group has dramatically decreased in use and fallen into regulatory disfavor because, in general, its structural properties promote both persistence in the environment and bioaccumulation within the food chain. In contrast the herbicide 2,4D contains carbon, hydrogen, chlorine, and oxygen, and is a widely used herbicide with environmental and toxicological properties distinctly different from the organochlorine insecticides. The organochlorine insecticides represent the first group of synthetic compounds to have a significant impact on the control of infectious diseases transmitted via insect vectors. These insecticides were used extensively in the United States and other Western countries, and are still used in Third World regions as both agricultural insecticides and agents to combat such vectorborne diseases as malaria, typhus, plague, Chagas' disease, yellow fever, dengue, encephalitis, filariasis, and African trypanosomiasis (sleeping sickness). Of these insecticides, DDT (dichlorodiphenyltrichloroethane) is credited as the primary compound that, for the first time in history, brought epidemics of malaria, typhus, and plague to a complete stop. DDT was introduced in 1943, with related insecticides following shortly thereafter. This chemical is still used extensively in tropical regions to combat malarial mosquitoes, and substitution of this pesticide with others such as malathion would be most expensive. One attribute that contributes to the effectiveness of this chemical class is its persistence in the environment, providing not only an immediate impact on insect populations but also a prolonged insecticidal presence extending well beyond the time of application. This persistence is now generally considered an undesirable feature owing to findings suggesting delayed adverse impacts on nontarget populations of insects as well as birds. In addition, increased cancer risks for humans are alleged to result from exposures to these chemicals such as those resulting from pesticide applications and ingestion of contaminated fish and other food species. Although the actual balance of risks versus benefits associated with the use of these insecticides is debated, regulatory action has virtually eliminated their use in the United States and other western countries. Summarizes the regulatory status of these products. The persistence of these insecticides in the environment and their prolonged activity against pests following application can be attributed to a combination of their insolubility in water and high solubility in fats, absorption and adsorption onto particulate matter, and resistance to chemical, physical, and microbiological degradation. From target crops and surrounding soil and water, these compounds have entered the food chains of mammals, birds, fishes, and other animal species. DDT in particular was implicated in inducing acute and perhaps chronic insecticide intoxications in fish and birds as a result of bioaccumulation. Smith discusses the fact that the primary acute toxicity noted in animals and humans following excessive exposures to chlorinated insecticides is neurological hyperactivity. With DDT and related compounds, the effects progress gradually from mild tremors to convulsions, whereas convulsions are the first sign of intoxication for compounds such as lindane, aldrin, dieldrin, endrin, toxaphene, and related materials. The latter can produce incoordination, weakness, and an ataxic state that is not associated with tremor, discriminating the intoxication induced by these substances from that of DDT. In general, the acute effects have not been shown to pose significant hazards to exposed populations, and current concern over the toxicities of these compounds is linked primarily to chronic low‐level exposures discussed below. As mentioned above, because of reported environmental effects of these pesticides plus their classifications in the early 1970s as “potential human carcinogens,” the use of most organochlorine pesticides was discontinued or markedly curtailed in the United States, Canada, and most European countries. The alleged human hazard, cancer, was based on observations of tumor induction in laboratory animals, primarily in mice, in which these compounds produced benign and malignant liver cell tumors. One reason for this debate is that few chemicals that induce rodent tumors appear to induce activity in humans. Frank and undisputed injury to the liver or other human organs has not been reported in the United States, Canadian, and Western European literature. To the best of our knowledge the organochlorine insecticides (individually and in combination) that have been ingested with home‐ and restaurant‐prepared food and drink by the U.S. population for more than 35 years (DDT was introduced in 1943), followed by a period of greatly reduced intake, have caused no recognized or clearly defined harmful effects. The significance of rodent liver tumors as indicators of human cancer risks continues to be debated in scientific circles. Parenthetically, although the organochlorine insecticides are considered potential human carcinogens. Although liver cancer death rates have declined, the incidence of human breast cancer has increased. This increased incidence of breast cancer was largely attributed to more frequent use of mammography and other screening techniques, as well as other changes in other risk factors such as prevalence of certain reproductive variables.

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Effect of aldrin on spermatogenesis, plasma gonadotrophins and testosterone, and testicular testosterone in the rat

Cited by 18 publications

References 25 publications

Study of quinalphos (an environmental oestrogenic insecticide) formulation (Ekalux 25 E.C.)-induced damage of the testicular tissues and antioxidant defence systems in Sprague-Dawley albino rats

Study of quinalphos (an environmental oestrogenic insecticide) formulation (Ekalux 25 E.C.)-induced damage of the testicular tissues and antioxidant defence systems in Sprague-Dawley albino rats

Environmental Factors That Disrupt Leydig Cell Steroidogenesis

Miscellaneous Chlorinated Hydrocarbon Pesticides

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