E J Sree Kumar, Aruna Parameswari, Akilandeswari Manickam, Makani Purva
Establishment of a simulation centre: Challenges and solutions
Indian journal of anaesthesia
bisphenola bpa influence male fertility mechanisms activated following bpa exposure bpa exposure causes hormonal disruption alters mitochondrial dynamics activity ultimately leading decreased male fertility public health concerns following bpa exposure rising globally need understand exact mechanisms bpa various diseases bpa exposure causes hormonal imbalances affects male fertility binding estrogen receptors ers mechanism mediates hormonal dysregulation yet studied study consisted comparative study using mice separated control group group exposed lowest observed adverse effect level loael n 20 micegroup week acclimatization environment study loael established us environmental protection agency 50 mgkg body weight bwday bpa used control mice given corn oil orally based daily variations bw groups gavaged every day 6 11 weeks 6week exposure sampling mice stabilized week testes spermatozoa mouse collected investigate effects bpa male fertility ivf carried using cumulusoocyte complexes female hybrid b6d2f1crljori mice n 3 ages eight twelve weeks signaling pathways apoptosis mitochondrial activitydynamicsrelated proteins evaluated western blotting elisa performed determine levels sex hormones fsh lh testosterone serum hematoxylin eosin staining used determine effects bpa histological morphology stage viiviii testicular seminiferous epithelium blastocyst formation cleavage development rate evaluated using ivf bpa acted binding ers g proteincoupled receptors activating protein kinase mitogenactivated protein kinase signaling pathways leading aberrant hormone levels effects respiratory chain complex atp synthase proteinrelated apoptotic pathways testis mitochondria p 005 subsequently embryo cleavage blastocyst formation reduced use affected sperm abnormal morphology seminiferous tubules stage vii viii seminiferous epithelial cells p 005 observed noteworthy histopathological lesions detected testes loael dose even though mice remained generally healthy exhibit significant changes bw following bpa exposure observations suggest testicular toxicity secondary outcome compromised overall health mice due systemic effects applicable since protein expression levels testes validated vitro studies testicular cell type leydig cells sertoli cells spermatogonial stem cells would required shed light exact mechanism resulting bpa exposure furthermore bpa doses employed study significantly exceed typical human exposure levels reallife scenarios consequently imperative conduct experiments focusing effects bpa concentrations line daily human exposures comprehensively assess impact testicular toxicity mitochondrial activity findings demonstrate bpa exposure impacts male fertility disrupting mitochondrial dynamics activities testes provides solid foundation subsequent investigations effects male reproductive function fertility following bpa exposure underlying mechanisms responsible effects addition findings suggest loael concentration bpa demonstrates exceptional toxicity especially considering specific impact testes adverse consequences male fertility impairing mitochondrial activity therefore plausible suggest bpa elicits distinct toxicological responses mechanistic endpoints based particular concentration levels target organ work supported basic science research program national research foundation korea nrf funded ministry education nrf2018r1a6a1a03025159 competing interests declared