PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10908312-5	2000	Treatment of hepatocytes with BHA also induced loss of mitochondrial transmembrane potential (Deltapsi(m)), cytochrome c, and activation of caspase-3, -8, and -9 but not caspase-1.	Butylated Hydroxyanisole	30-33	cytochrome c, somatic	Homo sapiens	108-120	
31381342-6	2019	BHA increased the levels of pro-apoptotic proteins, such as BAX, cytochrome c, cleaved caspase 3, and cleaved caspase 9, and decreased the level of anti-apoptotic protein BCL-XL.	Butylated Hydroxyanisole	0-3	cytochrome c, somatic	Homo sapiens	65-77	
10908312-6	2000	Pretreatment with cyclosporin A, an agent that stabilizes mitochondrial permeability transition pore, inhibited BHA-induced loss of Deltapsi(m), cytochrome c release, caspase activation, and apoptosis.	Butylated Hydroxyanisole	112-115	cytochrome c, somatic	Homo sapiens	145-157	
10908312-9	2000	Indeed, direct incubation of BHA with isolated mitochondria triggered cytochrome c release.	Butylated Hydroxyanisole	29-32	cytochrome c, somatic	Homo sapiens	70-82	
10908312-10	2000	Thus, these results indicate that the cytotoxicity of BHA is due to the induction of apoptosis that is mediated by the direct release of cytochrome c and the subsequent activation of caspases.	Butylated Hydroxyanisole	54-57	cytochrome c, somatic	Homo sapiens	137-149