Suppression of testicular steroidogenesis in rats by the organochlorine insecticide Aldrin.
TL;DR: HCG administration in the long-term treatment restored the steroidogenic enzymes activity and the nuclear diameter of the Leydig cells and reduced the accumulation of tissue cholesterol towards the vehicle-injected controls.
Abstract: Treatment with Aldrin, an organochlorine insecticide, for 13 and 26 days caused suppression of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activities, along with accumulation of cholesterol in the testicular tissues of adult rats. The same treatment also resulted in a reduction in the nuclear diameter of Leydig cells (LCND) and diameter of seminiferous tubules. A decrease in the weight of testes, seminal vesicles and ventral prostate was also noted. HCG administration in the long-term (26 days) treatment restored the steroidogenic enzymes activity and the nuclear diameter of the Leydig cells. It also reduced the accumulation of tissue cholesterol towards the vehicle-injected controls. The inhibition of steroidogenesis in the testes possibly reflects a decrease in pituitary gonadotrophin release after the treatment with Aldrin.
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TL;DR: The effects of some of the more commonly used environmental contaminants on testicular function through the induction of oxidative stress and apoptosis are discussed.
Abstract: Male reproductive health has deteriorated considerably in the last few decades. Nutritional, socioeconomic, lifestyle and environmental factors (among others) have been attributed to compromising male reproductive health. In recent years, a large volume of evidence has accumulated that suggests that the trend of decreasing male fertility (in terms of sperm count, quality and other changes in male reproductive health) might be due to exposure to environmental toxicants. These environmental contaminants can mimic natural oestrogens and target testicular spermatogenesis, steroidogenesis, and the function of both Sertoli and Leydig cells. Most environmental toxicants have been shown to induce reactive oxygen species, thereby causing a state of oxidative stress in various compartments of the testes. However, the molecular mechanism(s) of action of the environmental toxicants on the testis have yet to be elucidated. This review discusses the effects of some of the more commonly used environmental contaminants on testicular function through the induction of oxidative stress and apoptosis.
165 citations
TL;DR: The results indicate that nickel sulfate affects the steroidogenic enzymes, causing alteration in the formation of testosterone in both dietary groups, which was manifested in the elevated cholesterol and ascorbic acid level with decreased activities of steroidogenic enzyme in adult rats testes, but these alterations were reversible in both groups of animals fed normal protein diets and protein-restricted diets.
Abstract: Nickel, a widely used heavy metal, exerts potent toxic effects on peripheral tissues as well as on the reproductive system. Low dietary protein coupled with exposure to this metal induces more severe changes, including biochemical defects, structural disorders, and altered physiologic functions. This study was designed to assess the effects of nickel sulfate on testicular steroidogenesis and to ascertain whether such alterations are reversible with normal protein and protein-restricted dietary regime. Nickel sulfate [2 mg/100 g body weight (bw)] dissolved in double-distilled water was administered on alternate days for 10 doses in a normal protein diet (18% casein) and a protein-restricted diet (5% casein) to Wistar male albino rats (bw 160 +/- 5 g). Two groups, one with a normal protein diet and the other with a protein-restricted diet, served as controls. Twenty-four hours after the last treatment, all the animals except those in withdrawal groups were sacrificed by decapitation. We observed a significant reduction in the activities of the testicular steroidogenic enzymes and plasma testosterone concentration accompanied by a significant elevation in cholesterol and ascorbic acid level in both dietary groups. After 15 days of withdrawal from the nickel sulfate treatment, the testicular steroidogenic enzymes, along with plasma testosterone level, improved significantly in both normal protein-fed and protein-restricted dietary groups. The effects of nickel on testicular cholesterol and ascorbic acid concentration were also reduced after withdrawal. Our results indicate that nickel sulfate affects the steroidogenic enzymes, causing alteration in the formation of testosterone in both dietary groups, which was manifested in the elevated cholesterol and ascorbic acid level with decreased activities of steroidogenic enzymes in adult rats testes. However, these alterations were reversible in both groups of animals fed normal protein diets and protein-restricted diets.
66 citations
Cites background from "Suppression of testicular steroidog..."
...protein intake decreases synthesis of testicular enzymes, lowering the testosterone level, which is further aggravated by exposure of nickel (37)....
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TL;DR: The results suggest that prenatal exposure to OCPs disrupt reproductive hormones of fetuses in utero among boys, even at relatively low levels.
Abstract: Certain organochlorine pesticides (OCPs) are designated as persistent organic pollutants and are regulated in many countries. The effects of OCPs on pediatric endocrinology are a concern; however, only limited data exist from human studies on maternal OCP exposure and its effects on infants' hormone levels. This study was conducted as part of the Hokkaido Study Sapporo Cohort, a prospective birth cohort study in Japan. Participants included 514 women who enrolled at 23-35weeks of gestation between 2002 and 2005; maternal blood samples were collected in late pregnancy, and 29 OCPs were measured. Reproductive and steroid hormone levels in cord blood were also determined. Characteristics of mothers and their infants were obtained from self-administered questionnaires and medical records. Ultimately, 232 samples with both OCP and hormone data were analyzed. Fifteen of 29 investigated OCPs were detected in over 80% of the samples, with p,p'-dichlorodiphenyldichloroethylene showing the highest concentration (median value: 619pg/g-wet). The association between OCPs and sex hormone levels varied by sex. Linear regression models after sex stratification showed that chlordanes, cis-hexachlorobenzene, heptachlor epoxide, Mirex, and toxaphenes in maternal blood were inversely associated with testosterone, cortisol, cortisone, sex hormone-binding globin, prolactin, and androstenedione-dehydroepiandrosterone (DHEA) and testosterone-androstenediones ratios among boys. Furthermore, these OCPs were positively correlated with DHEA, follicle stimulating hormone (FSH), and adrenal androgen-glucocorticoid and FSH-inhibin B ratios among boys. In categorical quartile models, testosterone and DHEA were inversely and positively associated with OCPs, respectively. Estradiol-testosterone and adrenal androgen-glucocorticoid ratios tended to increase with increasing OCP concentrations in the higher quartile, while the testosterone-androstenedione ratio tended to decrease. Sex hormone-binding globulin and prolactin showed an inverse association with OCPs. Among girls, the linear regression model showed that only p,p'-dichlorodiphenyltrichloroethane was inversely associated with the level of DHEA and the adrenal androgen-glucocorticoid ratio, but was positively associated with cortisone levels. However, no associations were observed using the quartile categorical model. These results suggest that prenatal exposure to OCPs disrupt reproductive hormones of fetuses in utero among boys, even at relatively low levels.
41 citations
Cites result from "Suppression of testicular steroidog..."
...Decreasing testosterone-androstenedione ratio trends suggests the 428 downregulation of HSB17B1; previous animal studies have shown that aldrin inhibits 429 HSB17B1 (Chatterjee et al. 1988), which is consistent with our findings....
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...429 HSB17B1 (Chatterjee et al. 1988), which is consistent with our findings....
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TL;DR: It is suggested that quinalphos may have a suppressive influence on gonadotrophin release but its direct detrimental action at the level of the testes may also be responsible for the observed changes in spermatogenesis and in testicular testosterone production in rats.
Abstract: Quinalphos (O,O-diethyl-O-[quinoxalinyl-(2)-thionophosphate]) is a well-known organophosphorus insecticide used extensively in agriculture that adversely interferes with the activity of testicular steroidogenic enzymes in rats. To investigate its effects on spermatogenesis, the other function of testes, quantitative evaluation of different varieties of germ cells at stage VII of the seminiferous epithelium cycle, namely, type A spermatogonia (ASg), preleptotene spermatocytes (pLSc), midpachytene spermatcytes (mPSc), and step 7 spermatids (7Sd), along with the radioimmunoassay of plasma FSH, LH, testosterone, and testicular testosterone, were performed in Wistar rats following treatment with quinalphos (250 μg/kg, ip) for approximately one (13 days) and two cycles (26 days) of the seminiferous epithilium. Massive degeneration of all varieties of germ cells at stage VII, remarkable reduction in the sperm count, and significant reductions in plasma concentrations of FSH and testosterone, along with testicular testosterone, were observed after quinalphos treatment. Significant reduction in the plasma concentration of LH was observed only after treatment for two cycles. Administration of human chorionic gonadotrophin for 26 days in rats injected with quinalphos partially prevented the degeneration of germ cells and increased testosterone production. It is suggested that quinalphos may have a suppressive influence on gonadotrophin release but its direct detrimental action at the level of the testes may also be responsible for the observed changes in spermatogenesis and in testicular testosterone production in rats.
31 citations
TL;DR: It is suggested that quinalphos may exert a suppressive effect on the functional activity of accessory sex glands by decreasing testicular testosterone production following inhibition of pituitary gonadotrophins release.
Abstract: Biochemical estimation of prostatic acid phosphatase and fructose content in accessory sex glands, along with radioimmunoassay of plasma gonadotrophins (FSH and LH) and testosterone were performed in Wistar rats following treatment with quinalphos, an organophosphorus insecticide, for 13 and 26 days. Prostatic acid phosphatase activity and fructose content of the accessory sex glands, and plasma levels of testosterone and FSH were significantly lower in all rats treated with quinalphos. However, the degree of inhibition was more extensive in the 26 day-treatment group who, in addition also exhibited a significant reduction in relative weights of the testes and accessory sex organs, and plasma levels of LH. All these adverse effects of quinalphos were prevented when exogenous HCG was administered in concomitant with the insecticide for 26 days. These results suggest that quinalphos may exert a suppressive effect on the functional activity of accessory sex glands by decreasing testicular testosterone production following inhibition of pituitary gonadotrophins release.
31 citations
Cites background from "Suppression of testicular steroidog..."
...Previously we have noted that aldrin, an organochlorine insecticide, inhibits testicular testosterone production and spermatogenesis in rats by interfering with pituitary FSH and LH release ( Chatterjee et al. 1988, 1988a )....
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References
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Journal Article•
TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
Abstract: Since 1922 when Wu proposed the use of the Folin phenol reagent for the measurement of proteins, a number of modified analytical procedures utilizing this reagent have been reported for the determination of proteins in serum, in antigen-antibody precipitates, and in insulin. Although the reagent would seem to be recommended by its great sensitivity and the simplicity of procedure possible with its use, it has not found great favor for general biochemical purposes. In the belief that this reagent, nevertheless, has considerable merit for certain application, but that its peculiarities and limitations need to be understood for its fullest exploitation, it has been studied with regard to effects of variations in pH, time of reaction, and concentration of reactants, permissible levels of reagents commonly used in handling proteins, and interfering substances. Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
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TL;DR: A number of cases of infertility were discovered among men working in a California pesticide factory, and the suspected cause was exposure to the chemical 1,2-dibromo-3-chloropropane (D.B.C.P).
Abstract: A number of cases of infertility were discovered among men working in a California pesticide factory. The suspected cause was exposure to the chemical 1,2-dibromo-3-chloropropane (D.B.C.P.). The major effects, seen in 14 of 25 non-vasectomised men, were azoospermia or oligospermia and raised serum-levels of follicle-stimulating hormone and luteinising hormone. No other major abnormalities were detected, and testosterone levels were normal. Although a quantitative estimation of exposure could not be obtained, the observed effects appeared to be related to duration of exposure to D.B.C.P.
631 citations