PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28939271-7	2018	Signal transduction studies showed that PFOS exposure significantly elevated inducible nitric oxide synthase (iNOS), Bax, cytochrome c, cleaved caspase-9 and cleaved caspase-3, indicating the mitochondria-dependent apoptotic pathway was activated.	perfluorooctane sulfonic acid	40-44	BCL2 associated X, apoptosis regulator	Rattus norvegicus	117-120	
28985536-8	2018	At >= 500 nM, PFOS downregulated Lhcgr, inhibited BCL-2 and increased BAX levels to cause Leydig cell apoptosis.	perfluorooctane sulfonic acid	17-21	BCL2 associated X, apoptosis regulator	Rattus norvegicus	73-76	
24616003-8	2015	The mRNA and protein expression levels of p53, bax, cytochrome c, caspase-9, and caspase-3 in the offspring"s heart were enhanced in various PFOS-treated groups, meanwhile, the bcl-2 expression levels were decreased.	perfluorooctane sulfonic acid	141-145	BCL2 associated X, apoptosis regulator	Rattus norvegicus	47-50	
21440054-5	2012	The results showed that maternal exposure to 2.0mg/kgd PFOS caused severe histopathological changes along with marked oxidative injuries and cell apoptosis in offspring lungs; at the same time, the ratio of Bax to Bcl-2, release of cytochrome c (Cyt c) from mitochondria to cytoplasm, expressions of Fas and Fas-L, and activities of caspase-3, -8 and -9 were up-regulated correspondingly.	perfluorooctane sulfonic acid	55-59	BCL2 associated X, apoptosis regulator	Rattus norvegicus	207-210	
34815766-13	2022	The protein expressions profiles of p53 and Bax were also significantly upregulated in the 10 mg/kg PFOS group.	perfluorooctane sulfonic acid	100-104	BCL2 associated X, apoptosis regulator	Rattus norvegicus	44-47