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Repeated exposure to iron oxide nanoparticles causes testicular toxicity in mice
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ABSTRACTThe aim of this study was to determine whether repeated exposure to iron oxide nanoparticles (Fe2O3‐NPs) could be toxic to mice testis. Fe2O3‐NPs (25 and 50 mg/kg) were intraperitoneally administered into mice once a week for 4 weeks. Our study showed that Fe2O3‐NPs have the ability to cross the blood‐testis barrier to get into the testis. The findings showed that exposure resulted in the accumulation of Fe2O3‐NPs which was evidenced from the iron content and accumulation in the testis. Furthermore, 25 and 50 mg/kg Fe2O3‐NPs administration increased the reactive oxygen species, lipid peroxidation, protein carbonyl content, glutathione peroxidase activity, and nitric oxide levels with a concomitant decrease in the levels of antioxidants—superoxide dismutase, catalase, glutathione, and vitamin C. Increased expression of Bax, cleaved‐caspase‐3, and cleaved‐PARP confirms apoptosis. Serum testosterone levels increased with increased concentration of Fe2O3‐NPs exposure. In addition, the histopathological lesions like vacuolization, detachment, and sloughing of germ cells were also observed in response to Fe2O3‐NPs treatment. The data from our study entailed that testicular toxicity caused by Fe2O3‐NPs exposure may be associated with Fe2O3‐NPs accumulation leading to oxidative stress and apoptosis. Therefore, precautions should be taken in the safe use of Fe2O3‐NPs to avoid complications in the fertility of males. Further research will unravel the possible molecular mechanisms on testicular toxicity of Fe2O3‐NPs. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 594–608, 2017.
Title: Repeated exposure to iron oxide nanoparticles causes testicular toxicity in mice
Description:
ABSTRACTThe aim of this study was to determine whether repeated exposure to iron oxide nanoparticles (Fe2O3‐NPs) could be toxic to mice testis.
Fe2O3‐NPs (25 and 50 mg/kg) were intraperitoneally administered into mice once a week for 4 weeks.
Our study showed that Fe2O3‐NPs have the ability to cross the blood‐testis barrier to get into the testis.
The findings showed that exposure resulted in the accumulation of Fe2O3‐NPs which was evidenced from the iron content and accumulation in the testis.
Furthermore, 25 and 50 mg/kg Fe2O3‐NPs administration increased the reactive oxygen species, lipid peroxidation, protein carbonyl content, glutathione peroxidase activity, and nitric oxide levels with a concomitant decrease in the levels of antioxidants—superoxide dismutase, catalase, glutathione, and vitamin C.
Increased expression of Bax, cleaved‐caspase‐3, and cleaved‐PARP confirms apoptosis.
Serum testosterone levels increased with increased concentration of Fe2O3‐NPs exposure.
In addition, the histopathological lesions like vacuolization, detachment, and sloughing of germ cells were also observed in response to Fe2O3‐NPs treatment.
The data from our study entailed that testicular toxicity caused by Fe2O3‐NPs exposure may be associated with Fe2O3‐NPs accumulation leading to oxidative stress and apoptosis.
Therefore, precautions should be taken in the safe use of Fe2O3‐NPs to avoid complications in the fertility of males.
Further research will unravel the possible molecular mechanisms on testicular toxicity of Fe2O3‐NPs.
© 2016 Wiley Periodicals, Inc.
Environ Toxicol 32: 594–608, 2017.
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