PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2609348-7	1989	These results suggest that the reductive activation to free radicals, catalyzed by cytochrome P-450, and thus the induction of lipid peroxidation at low but physiological PO2 are characteristic not only of CCl4 but also of other polyhalogenated methanes, especially CBrCl3, CBr4, CHI3, CHBr3, and CHBr2Cl.	PO-2	171-174	C-C motif chemokine ligand 4	Rattus norvegicus	206-210	
3401014-9	1988	These results provide further evidence for the decisive role of lipid peroxidation, preferentially induced at low PO2, in CCl4 liver injury.	PO-2	114-117	C-C motif chemokine ligand 4	Rattus norvegicus	122-126	
3508440-3	1987	Monitoring of hepatocellular oxygen uptake, malondialdehyde-formation and low-level chemiluminescence during incubations of CCl4-supplemented hepatocytes indicated a drastic stimulation of lipid peroxidation at pO2-levels between 1 and 10 mmHg.	PO-2	211-214	C-C motif chemokine ligand 4	Rattus norvegicus	124-128	
3508440-5	1987	The evaluation of cellular damages by determining trypan blue exclusion and lactate dehydrogenase leakage revealed that in the presence of CCl4 hepatocellular injury was significantly increased at those pO2-levels which were optimal for CCl4-mediated lipid peroxidation.	PO-2	203-206	C-C motif chemokine ligand 4	Rattus norvegicus	139-143	
3508440-5	1987	The evaluation of cellular damages by determining trypan blue exclusion and lactate dehydrogenase leakage revealed that in the presence of CCl4 hepatocellular injury was significantly increased at those pO2-levels which were optimal for CCl4-mediated lipid peroxidation.	PO-2	203-206	C-C motif chemokine ligand 4	Rattus norvegicus	237-241	
3508440-6	1987	The present results demonstrate that CCl4 is a potent inducer of lipid peroxidation also in the intact hepatocyte, provided that the pO2 is maintained at distinct low levels.	PO-2	133-136	C-C motif chemokine ligand 4	Rattus norvegicus	37-41	
6477950-3	1984	Under these conditions, at the hypoxic end of the physiological PO2 in liver, CCl4 caused a 5-fold increase in the oxygen uptake rate and a 20-fold increase in the malondialdehyde formation rate while, at 80 mmHg (10.7 kPa) the haloalkane caused only an increase of 2- and 4-fold, respectively; in comparison, there was only a slight increase in NADPH-induced lipid peroxidation with increasing PO2.	PO-2	64-67	C-C motif chemokine ligand 4	Rattus norvegicus	78-82	
6477950-3	1984	Under these conditions, at the hypoxic end of the physiological PO2 in liver, CCl4 caused a 5-fold increase in the oxygen uptake rate and a 20-fold increase in the malondialdehyde formation rate while, at 80 mmHg (10.7 kPa) the haloalkane caused only an increase of 2- and 4-fold, respectively; in comparison, there was only a slight increase in NADPH-induced lipid peroxidation with increasing PO2.	PO-2	395-398	C-C motif chemokine ligand 4	Rattus norvegicus	78-82	
6477950-4	1984	These data clearly demonstrate the critical role of low steady-state PO2 in CCl4-induced lipid peroxidation and support lipid peroxidation as a key factor in CCl4 hepatotoxicity.	PO-2	69-72	C-C motif chemokine ligand 4	Rattus norvegicus	76-80