Effect of Bisphenol S on testicular tissue after low-dose lactation exposure
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články
PubMed
36096261
DOI
10.1016/j.envpol.2022.120114
PII: S0269-7491(22)01328-8
Knihovny.cz E-zdroje
- Klíčová slova
- Bisphenol S, Blood-testis barrier, Idiopathic infertility, Lactation exposure, Oxidative stress, Testicular tissue,
- MeSH
- benzhydrylové sloučeniny toxicita MeSH
- endokrinní disruptory * toxicita MeSH
- laktace * MeSH
- myši MeSH
- sulfony toxicita MeSH
- testis MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- benzhydrylové sloučeniny MeSH
- bisphenol S MeSH Prohlížeč
- endokrinní disruptory * MeSH
- sulfony MeSH
Exposure to endocrine disruptors such as bisphenols, can lead to and be the explanation for idiopathic infertility. In our study, we assessed the effect of exposure to bisphenol S (BPS) via breast milk on the testicular tissue health of adult male mice. Lactating dams were exposed to BPS through drinking water (0.216 ng g bw/day and 21.6 ng g bw/day) from post-natal day 0-15. Although there was no significant difference in testicular histopathology between the control and experimental groups, we observed an increase in the number of tight and gap junctions in the blood-testis barrier (BTB) of adult mice after lactation BPS exposure. Moreover, there was an increase in oxidative stress markers in adult testicular tissue of mice exposed via breast milk. Our lactation model indicates that breast milk is a route of exposure to an endocrine disruptor that can be responsible for idiopathic male infertility through the damage of the BTB and weakening of oxidative stress resistance in adulthood.
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