Early exposure to paracetamol reduces level of testicular testosterone and changes gonadal expression of genes relevant for steroidogenesis in rats offspring.
Kamilla Blecharz-KlinAnna Sznejder-PachołekAdriana WawerJustyna PyrzanowskaAgnieszka PiechalIlona Joniec-MaciejakDagmara Mirowska-GuzelEwa Widy-TyszkiewiczPublished in: Drug and chemical toxicology (2021)
In this study, we investigated the effects of early paracetamol treatment on the testicular level of testosterone and expression of genes important for steroid biosynthesis and reproduction in male rats offspring. Rats were continuously exposed to paracetamol at doses of 5 or 15 mg/kg b.w. during pregnancy and the first two months of the postpartum development. Testosterone level was determined by ELISA. Profile of gene expression for the testicular steroidogenic factors were evaluated using the Real-Time PCR. Our results showed that paracetamol reduces testicular testosterone level and causes compensatory transactivation of genes important for steroidogenesis and reproductive capacity. We have observed significant over-expression of several genes involved in cholesterol transport and steroid biosynthesis e.g., genes for steroidogenic acute regulatory protein, hydroxysteroid dehydrogenases, luteinizing hormone subunit beta, gonadotropin and androgen receptors. Up-regulation of these genes with parallel testosterone reduction in the testicles could be the possible mechanism that maintains and prevents the loss of the steroidogenic function.
Keyphrases
- replacement therapy
- genome wide
- poor prognosis
- gene expression
- bioinformatics analysis
- genome wide identification
- germ cell
- binding protein
- genome wide analysis
- real time pcr
- smoking cessation
- long non coding rna
- type diabetes
- transcription factor
- liver failure
- intensive care unit
- mouse model
- high resolution
- amino acid
- monoclonal antibody
- cell wall