Environmentally relevant DEHP exposure during gestational and lactational period inhibits filamin a testicular expression.
Pablo A PérezJonathan ToledoFacundo VitelliniVictoria Navall CuelloVerónica CantarelliMarina PonzioJorge H MukdsiSilvina GutiérrezPublished in: Journal of molecular histology (2023)
Toxicological studies have revealed that DEHP exposure during pregnancy may induce developmental disorders, especially in male offspring, leading to morphological and functional alterations in the reproductive system by mechanisms that should be investigated. Thus, the aim of this work was to analyze the testicular toxicity induced by an environmentally relevant DEHP dose during development and its impact on FLNA, a protein that participates in the blood-testis barrier assembly. We used male Wistar rats exposed to DEHP during pregnancy and lactation. The results showed that DEHP exposure during development and lactation increased body weight, decreased gonadal weight and shortened anogenital distance. This phthalate induced morphological changes in the testis, suggestive of hypospermatogenesis. DEHP exposure decreased the number of FLNA positive cells and the expression of FLNA and claudin-1 in prepubertal testes. Furthermore, DEHP inhibited FLNA and claudin-1 protein expression in adult male rats. These results indicated that exposure to DEHP during gestation and lactation perturbed testis development and suggested that FLNA is a target protein of DEHP, possibly contributing to the phthalate-induced damage on BTB.
Keyphrases
- body weight
- poor prognosis
- germ cell
- oxidative stress
- binding protein
- weight gain
- dairy cows
- high glucose
- diabetic rats
- induced apoptosis
- pregnant women
- metabolic syndrome
- type diabetes
- high fat diet
- adipose tissue
- endothelial cells
- long non coding rna
- physical activity
- protein protein
- amino acid
- weight loss
- drug induced
- small molecule
- high resolution
- birth weight