transcripts, with corresponding decreases in AGTR1A, CYP11B2, and IGF1 protein expression, implicating disrupted hormone biosynthesis and adrenal growth signaling. In H295R cells, LCT at ≤1000 μM was noncytotoxic but suppressed aldosterone and cortisol secretion at 100 μM. This concentration also significantly inhibited AGTR1A and CYP11B2 expression, increased CASP3, and decreased BCL-2 levels, without changes in ROS generation or mitochondrial membrane potential, suggesting apoptosis induction through ROS- and MMP-independent pathways. Collectively, these findings reveal that LCT impairs adrenal endocrine development and function by downregulating key steroidogenic mediators and promoting apoptosis.
Chen et al. (Fri,) studied this question.