Effect of atenolol on cadmium-induced testicular toxicity in male rats

Biswas, N. M.; Gupta, Ranojoy Sen; Chattopadhyay, Alok; Choudhury, Gargi Roy; Sarkar, M. A. R.

doi:10.1016/s0890-6238(01)00184-8

Cited by 78 publications

(52 citation statements)

References 17 publications

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“…Similar results were obtained by Pillai et al [5] after gestational and lactational exposure to Cd. Reduction in testicular weight has been, partly, attributed to the necrotic and degenerative Cd-induced changes [41,42]. Lower serum testosterone levels noted in Cd-exposed animals might be due to the direct effect of Cd on Leydig cells [43][44][45] or to an indirect effect by altering gonadotrophin from pituitary, because Cd have been shown to accumulate in the hypothalamus and the pituitary [46].…”

Section: Discussionmentioning

confidence: 99%

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Chemek

Mimouna

Boughammoura

et al. 2016

Reproductive Toxicology

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Highlights Effects of Cd and Zn on testicular development were assessed. Cd accumulation and Zn depletion in testis during lactation were noted. Cd-induced abnormal seminiferous tubules and a plasmatic testosterone decrease. Zn supply induced a significant protection against Cd toxicity. Cd toxicity observed in pups is mediated by disruption of maternal Zn metabolism. *Research Highlights AbstractTo assess the effects of exposure to Cd and Zn on rat testicular development, offspring, from mothers receiving either tap water, Cd, Zn or Cd+Zn during gestation and lactation periods, were observed on gestational day (GD) 20 and on postnatal days (PND) 12, 21 and 35. During gestation, Cd induced maternal hypozincemia and less transfer of Zn to the fetus. During lactation, progressive Cd accumulation and Zn depletion in testis at PND12 and PND21 werenoted. An increase of abnormal seminiferous tubules and a decrease in testis weight and plasmatic testosterone concentration were also observed at PND21 and PND35 respectively. Interestingly, Zn supply induced a significant protection against Cd toxicity. These results suggest that the toxic effects of Cd observed during development are mediated by the disruption of Zn metabolism, which is established in mothers during pregnancy causing Zn deficiency in fetuses and continues to become more pronounced during lactation.

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Section: Discussionmentioning

confidence: 99%

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Chemek

Mimouna

Boughammoura

et al. 2016

Reproductive Toxicology

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“…Androgen levels and the activity of 17β-HSD in cultured Leydig cells obtained from testes of male inbred KP mice after a single injection of CdCl 2 showed a marked decrease of activity of dehydrogenase; also, the androgen level decreased after Cd 2+ administration (Godowicz and Bilinska 1981). Biswas et al (2001) reported that in adult Sprague-Dawley male rats, Cd 2+ -induced stress adversely affected testicular activity by decreasing testicular ∆(5)-3β-HSD and 17β-HSD activities as well as serum testosterone and accessory sex organ weight. Mukherjee et al (1992) observed that isolated ovarian tissues from the common carp, Cyprinus carpi, incubated with CdCl 2 were impaired by gonadotropin-induced fish ovarian steroidogenesis; 17β-HSD activity was particularly affected.…”

Section: Discussionmentioning

confidence: 99%

Estradiol uptake, toxicity, metabolism, and adverse effects on cadmium-treated amphibian embryos.

Fridman

Corró

Herkovits

2004

Environ Health Perspect

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The exposure of Bufo arenarum embryos to 25 µmol/L 17β-estradiol (E 2 ) resulted in 100% lethality within 48 hr, whereas 10 µmol//L E 2 was the no observed effect concentration value for shortterm chronic (7 days) exposure. The toxicity profile curves show that lethal effects were proportional to the E 2 concentration and the time of exposure. The E 2 uptake resulted in 20.1 ng E 2 /mg embryo at 8 hr posttreatment, but 67.3% of this value was achieved during the first 30 min of incubation with this estrogen. Regarding metabolism, the embryos synthesize estrone (E 1 ) from E 2 by means of 17β-hydroxysteroid dehydrogenase. Simultaneous treatments of Bufo arenarum embryos with 1 mg/L Cd 2+ and 0.1, 1, or 10 µmol/L E 2 enhanced the lethality exerted by cadmium in 76.7, 80, and 83.3% of embryos, respectively. The results indicate that estrogenic endocrine disruptors could have an adverse effect on amphibian embryos and enhance the toxic effect of Cd on amphibian embryos. This study points to the possibility of using the AMPHITOX test as a screening method for potential endocrine disruption as well as the combined effects of chemical mixtures.

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“…Many studies indicate that Cd induces testicular damage in many species of animals, including mice, hamsters, rabbits, guinea pigs and dogs [1,2]. Cadmium has a profound effect on sex organ weight, which is the primary indicator of possible alteration in androgen status [3]. It can also, directly inhibit primary Leydig cell testosterone levels but the mechanism of this effect is unknown [4].…”

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confidence: 99%

Preventive Effect of Zinc Against Cadmium-induced Oxidative Stress in the Rat Testis

Abdelmelek²,

et al. 2008

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Abstract. The aim of this study was to investigate the antioxidant role of zinc (Zn) in the Cd-exposed testes of Wistar rats. Subchronic exposure to Cd (CdCl2, 40 mg/l, per os) for 30 days resulted in a significant reduction in growth rate (-11%) and relative weights of testes (-36%) and seminal vesicles (-80%). Treated rats displayed a decrease in testicular and plasma testosterone levels, respectively (-70%, P<0.05; -48%, P<0.05), epididymal sperm count (-22%, P<0.05), and spermatozoa motility (-35%, P<0.05). In contrast, Cd increased the malondialdehyde (+46%, P<0.05), metallothionein (+200%, P<0.05), and 8-oxodGuo concentrations (+71%, P<0.05) in the testis. In the gonad, Cd decreased the GPx (-30%, P<0.05), CAT (-32%, P<0.05), mitochondrial Mn-SOD (-34%, P<0.05), and cytosolic CuZn-SOD (-32%, P<0.05) activities. Zinc supplementation (ZnCl2, 40 mg/l, per os) in the Cd-exposed rats restored the activities of GPx, CuZn-SOD, and Mn-SOD in the testes to the levels of the control group. Moreover, zinc administration was capable of reducing the elevated levels of malondialdehyde in the testis. Interestingly, zinc supplementation attenuated DNA oxidation induced by Cd in the gonad and restored the testosterone level and sperm count to the levels of the control group. Zinc administration minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by Cd in the rat testis.

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Effect of atenolol on cadmium-induced testicular toxicity in male rats

Cited by 78 publications

References 17 publications

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Estradiol uptake, toxicity, metabolism, and adverse effects on cadmium-treated amphibian embryos.

Preventive Effect of Zinc Against Cadmium-induced Oxidative Stress in the Rat Testis

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