Pentabromophenol (NSC-5717) suppressed TGF-β response by accelerating the turnover rate of TGF-β receptors.

Following 18hr exposure of murine BV-2 cells, at dose levels resulting in ≥80% viability (10 and 40 μM), limited alterations in pro-inflammatory responses were observed however, changes were observed in mitochondrial respiration. Basal respiration, ATP-linked respiration, maximum respiration, basal glycolytic and compensatory glycolysis were altered by Pentabromophenol. Phagocytosis was decreased for Pentabromophenol and TBBPA. NLRP3 inflammasome activation was assessed using BV-2-ASC (apoptosis-associated speck-like protein containing a CARD) reporter cells to visualize aggregate formation. Pentabromophenol, showed a direct stimulation of aggregate formation and properties as a NLRP3 inflammasome secondary trigger[1].