PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
3653925-1	1987	Previous work on the mechanism of tumour-cell killing by the macrophage product tumour necrosis factor (TNF) is consistent with a free radical-induced process.	Free Radicals	130-142	tumor necrosis factor	Mus musculus	80-102	
2745981-3	1989	Both iron chelators and free radical scavengers inhibited this enhanced secretion of TNF, implying the involvement of free radicals via a Fenton-type reaction.	Free Radicals	118-131	tumor necrosis factor	Mus musculus	85-88	
3653925-1	1987	Previous work on the mechanism of tumour-cell killing by the macrophage product tumour necrosis factor (TNF) is consistent with a free radical-induced process.	Free Radicals	130-142	tumor necrosis factor	Mus musculus	104-107	
3653925-2	1987	In this study, free-radical involvement was sought by (i) investigating the effects on TNF cytolysis of anaerobic conditions, free-radical scavengers and inhibitors of two potential pathways of free-radical generation (oxidative phosphorylation and arachidonate metabolism) and (ii) looking for increased malonyldialdehyde (MDA) production in TNF-treated cells (MDA is a free radical-induced lipid peroxidation product).	Free Radicals	15-27	tumor necrosis factor	Mus musculus	87-90	
3653925-2	1987	In this study, free-radical involvement was sought by (i) investigating the effects on TNF cytolysis of anaerobic conditions, free-radical scavengers and inhibitors of two potential pathways of free-radical generation (oxidative phosphorylation and arachidonate metabolism) and (ii) looking for increased malonyldialdehyde (MDA) production in TNF-treated cells (MDA is a free radical-induced lipid peroxidation product).	Free Radicals	15-27	tumor necrosis factor	Mus musculus	343-346	
23082993-2	2013	Both cellular and cell-free tests show that carbon associated to quartz completely inhibits the typical free radical generation of quartz dusts (through Fenton activity and homolytic cleavage of a C-H bond) and suppresses the oxidative stress and inflammation induced by quartz alone on MH-S murine macrophage cells (lipid peroxidation, nitric oxide release, and tumor necrosis factor-alpha synthesis).	Free Radicals	104-116	tumor necrosis factor	Mus musculus	363-390	
22343416-4	2012	The free radical-mediated oxidation of cellular macromolecules, which was NADPH oxidase and P2X7 receptor-dependent, correlated well with the release of TNF-alpha and MCP-2 from Kupffer cells.	Free Radicals	4-16	tumor necrosis factor	Mus musculus	153-162	
15046874-2	2004	The mechanisms by which TNF reduces neuronal loss after brain injury may involve the up-regulation of proteins that maintain calcium homeostasis or reduce free radical generation.	Free Radicals	155-167	tumor necrosis factor	Mus musculus	24-27	
11679964-3	2001	With this model, it is now possible to evaluate whether free radicals are directly toxic or act as redox regulators of TNF-alpha production.	Free Radicals	56-69	tumor necrosis factor	Mus musculus	119-128	
11018074-7	2000	These data strongly support the hypothesis that free radicals from NADPH oxidase in hepatic Kupffer cells play a predominant role in the pathogenesis of early alcohol-induced hepatitis by activating NF-kappaB, which activates production of cytotoxic TNF-alpha.	Free Radicals	48-61	tumor necrosis factor	Mus musculus	250-259	
10336540-8	1999	Because tepoxalin suppresses the release of free radicals, PDTC scavenges free radicals and Bcl-2 is an antioxidant protein, free radicals are among the key mediators of this TNF-induced killing event.	Free Radicals	44-57	tumor necrosis factor	Mus musculus	175-178	
10336540-8	1999	Because tepoxalin suppresses the release of free radicals, PDTC scavenges free radicals and Bcl-2 is an antioxidant protein, free radicals are among the key mediators of this TNF-induced killing event.	Free Radicals	74-87	tumor necrosis factor	Mus musculus	175-178