TBPH

TBPH is a brominated flame retardant. TBPH enhances hepatic steatosis, inflammation, and fibrosis in mice with nonalcoholic steatohepatitis (NASH). TBPH induces dysregulation of phospholipid metabolism, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH leads to impaired endoplasmic reticulum-mitochondria (ER-Mito) contacts, subsequently causing mitochondrial dysfunction. TBPH induces lung injury through an inflammatory response mediated by mitochondria-derived ds-DNA. TBPH can be used to study the role of MFN2-mediated ER-mitochondria contacts in lipid metabolism homeostasis^[1][2]. In Vitro: TBPH (5-50 μM, 48 h) promotes NASH progression by disrupting MFN2-regulated ER-Mito contacts in NASH LOs model^[1].
TBPH (0-20 μg/mL, 48 h) decreases cell proliferation ability, causes oxidative stress, increase lung tissue fibrosis, causes the release of ds-DNA from lung mitochondria, which activates c-GAS-STING in TC-1 and BEAS-2B cells^[2]. In Vivo: TBPH (20-200 mg/kg, i.g., once a day, 4 weeks) enhances hepatic lipid accumulation and metabolic dysfunction, accelerates inflammatory responses and fibrotic progression, disrupts hepatic phospholipid homeostasis and hepatocytic ER-Mito contacts, induces mitochondrial dysfunction and ER stress, in the liver in methionine-choline-deficient (MCD) diet-induced NASH mouse model^[1].
TBPH (20-200 mg/kg, i.g., once a day, 4 weeks) does not alter liver morphology and does not change the hepatosomatic index, but impairs hepatocytic ER-Mito contacts, induces mitochondrial dysfunction and ER stress in normal diet (ND) mice model^[1].
TBPH (0-100 μg/mL, i.g., once a day, 4 weeks) causes oxidative damage to lung cells and triggers inflammatory responses in lung cells and tissues in C57 mice^[2].