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1.
Reprod Toxicol ; 129: 108669, 2024 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-39038765

RESUMEN

The present study investigated the possible effects of copper nanoparticles (CuNPs) after discontinuing treatment on testicular activity in a mouse model. The male mice were given continuous CuNPs treatment for 70 days and left untreated for 70 days. The results show that even after the discontinuation of CuNPs treatment, the testicular impairment was persistent till 140 days at a higher dose (200 mg/kg group). The spermatogenesis, sperm parameters, proliferation and antioxidant status were suppressed in the higher dose groups. However, these effects were also observed at moderate levels in the other CuNPs treated groups, such as at 10 mg/kg and 100 mg/kg. The apoptosis was stimulated at a higher dose compared to the other groups. The testosterone, LH levels and AR expression were suppressed in all the CuNPs treated groups, along with slight elevation in the estrogen levels and up-regulated ERß expression. The fertility data also showed a decline in all CuNPs treated groups with the lowest litter size in the 200 mg/kg treated group. Despite testis, epididymis and accessory sex organs like prostate, seminal vesicle, and vas deferens, histoarchitecture also showed impairment. This is the first report on how CuNPs affect the male reproductive system in mice even after treatment was terminated. The current study also demonstrated possible negative effects on male reproductive function that might last for longer at higher dosages of chronic CuNPs exposure even after termination.


Asunto(s)
Apoptosis , Cobre , Hormona Luteinizante , Nanopartículas del Metal , Espermatogénesis , Testículo , Testosterona , Animales , Masculino , Testículo/efectos de los fármacos , Testículo/metabolismo , Testículo/patología , Espermatogénesis/efectos de los fármacos , Testosterona/sangre , Apoptosis/efectos de los fármacos , Hormona Luteinizante/sangre , Cobre/toxicidad , Nanopartículas del Metal/toxicidad , Ratones , Espermatozoides/efectos de los fármacos , Fertilidad/efectos de los fármacos , Femenino , Receptores Androgénicos/metabolismo , Proliferación Celular/efectos de los fármacos
2.
J Exp Zool A Ecol Integr Physiol ; 341(2): 138-150, 2024 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-38047873

RESUMEN

Although the usage of nanoparticles has expanded substantially in recent years, and it causes the detrimental effect on the various organs. CuNPs are widely used in commercial applications. There has been minimal investigation into the possibly harmful effects of CuNPs on the accessory reproductive organs. Thus, the present study aimed to investigate the effect of CuNPs on the male reproductive organs like epididymis, vas deferens, seminal vesicle and prostate of mice. The mice were exposed orally to CuNPs at three doses 10, 100, and 200 mg/kg for 70 days. Our results showed that the organs index of only vas deferens and prostate reduced at 200 mg/kg group compared to the control. However, the histological study showed degenerative changes in the epididymis at higher doses like distortion in the tubules. The sperm parameters were also decreased in the 200 mg/kg CuNPs group. The vas deferens in 100 and 200 mg/kg treatment groups exhibited detachment of luminal epithelium and with a few or no spermatozoa in the higher dose group. The seminal vesicle and prostate also showed degenerative changes like atrophy, hyperplasia, and scant secretary materials. Furthermore, CuNPs also increased the oxidative stress and decreased antioxidant enzymes in vas deferens and seminal vesicles at higher dose. Caput epididymis showed decreased GPx enzymes in all the groups. However, MDA and GPx in corpus, cauda, and prostate did not show any significant variations among all the groups. In conclusion, our results suggest that CuNPs can manifest the detrimental effect of the male accessory organs and epididymis in a dose and tissue dependent manner. Since, detrimental effects were observed only at higher dose, thus, uses of CuNPs would be safe for reproductive organs at lower dose, even for the prolonged duration.


Asunto(s)
Cobre , Epidídimo , Masculino , Ratones , Animales , Epidídimo/patología , Cobre/farmacología , Semen , Conducto Deferente/patología , Próstata/patología
3.
J Biochem Mol Toxicol ; 37(9): e23400, 2023 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-37335250

RESUMEN

Cadmium (Cd) is one of the heavy metal pollutants present in the environment due to human intervention. It is well known that Cd causes toxicological effects on various organs, including the testes. Morin hydrate is a plant-derived bioflavonoid with antioxidant, anti-inflammatory, and anti-stress properties. Thus, the question can be raised as to whether Morin has an effect on Cd-intoxication-induced testicular impairment. Therefore, the aim of this study was to investigate the role of Morin on Cd-mediated disruption of testicular activity. Mice were divided into three groups: group 1 served as the control group, group 2 was given Cd (10 mg/kg) orally for 35 days, and group 3 was given Cd and Morin hydrate (100 mg/kg) for 35 days. To validate the in vivo findings, an in vitro study on testicular explants was also performed. The results of the in vivo study showed that Cd-intoxicated mice had testicular disorganization, reduced circulating testosterone levels, decreased sperm density, and elevated oxidative stress and sperm abnormality. The expression of the germ cell proliferation marker, germ cell nuclear acidic protein (GCNA), and adipocytokine visfatin were also downregulated. It was observed that Morin hydrate upregulated testicular visfatin and GCNA expression in Cd-intoxicated mice, along with improvement in circulating testosterone, testicular histology, and sperm parameters. Furthermore, the in vitro study showed that Cd-mediated downregulation of testicular visfatin and GCNA expression, along with the suppressed secretion of testosterone from testicular explants, was normalized by Morin treatment, whereas visfatin expression was not. Overall, these data indicate that environmental cadmium exposure impairs testicular activity through downregulation of visfatin and GCNA expression, and Morin might play a protective role against Cd-induced testicular toxicity.


Asunto(s)
Intoxicación por Cadmio , Testículo , Humanos , Masculino , Ratones , Animales , Testículo/metabolismo , Cadmio/toxicidad , Nicotinamida Fosforribosiltransferasa/metabolismo , Nicotinamida Fosforribosiltransferasa/farmacología , Semen/metabolismo , Antioxidantes/farmacología , Antioxidantes/metabolismo , Estrés Oxidativo , Testosterona/farmacología , Flavonoides/farmacología , Flavonoides/metabolismo , Intoxicación por Cadmio/metabolismo , Proliferación Celular
4.
Nanotoxicology ; 16(5): 658-678, 2022 06.
Artículo en Inglés | MEDLINE | ID: mdl-36256793

RESUMEN

Although copper is an indispensable trace metal for biological functions, its excess exposure causes hazardous effects on health. Copper in the form of nanoparticles (CuNPs) is widely used at present and therefore, the living organism is at continuous risk of its adverse effect. The prolonged treatment of CuNPs has not been evaluated yet on the male reproductive system. To demonstrate the combined adverse effects and the mechanism of copper nanoparticles (CuNPs), three doses of CuNPs, 10, 100 and 200 mg/kg were orally given to mice for 70 days. The present study demonstrated that CuNPs decreased the sperm quality parameters, male circulating hormones, induces testicular damages, increased oxidative stress, apoptosis, decreases antioxidant enzymes, germ cell proliferation, and increases the expression of 8-oxoguanine DNA glycosylase-1 (OGG1), apelin receptor (APJ) as well. CuNPs also down-regulated the expression of AR and Erα in the testis. These results suggest that CuNPs manifested their adverse effect on testis via modulating steroid and cytokine (apelin) receptors. The adverse effect of testis was most pronounced at the highest dose (200 mg/kg) of CuNPs, however, other doses show a less toxic effect on various parameters. In conclusion, results indicated that CuNPs may impair spermatogenesis via oxidative stress-mediated DNA damage and germ cell apoptosis at high doses.


Asunto(s)
Nanopartículas del Metal , Receptores de Esteroides , Masculino , Animales , Ratones , Cobre , Testículo , Nanopartículas del Metal/toxicidad , Semen , Espermatogénesis , Proliferación Celular , Receptores de Esteroides/metabolismo
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