PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31102529-4	2019	OBJECTIVES: To test whether physiological concentrations of N-acetylcysteine, a clinically safe antioxidant drug currently used in human therapy, is able to reduce ROS production, SOS induction and mutagenesis in ciprofloxacin-treated bacteria without affecting antibiotic activity.	Acetylcysteine	60-76	xylosyltransferase 2	Homo sapiens	180-183	
31102529-7	2019	RESULTS: Treatment with N-acetylcysteine reduced intracellular ROS levels (by ~40%), as well as SOS induction (by up to 75%) and bacterial filamentation caused by subinhibitory concentrations of ciprofloxacin, without affecting ciprofloxacin antibacterial activity.	Acetylcysteine	24-40	xylosyltransferase 2	Homo sapiens	96-99	
31102529-8	2019	Remarkably, N-acetylcysteine completely abolished SOS-mediated mutagenesis.	Acetylcysteine	12-28	xylosyltransferase 2	Homo sapiens	50-53	
31102529-9	2019	CONCLUSIONS: Collectively, our data strongly support the notion that ROS are a key factor in antibiotic-induced SOS mutagenesis and open the possibility of using N-acetylcysteine in combination with antibiotic therapy to hinder the development of antibiotic resistance.	Acetylcysteine	162-178	xylosyltransferase 2	Homo sapiens	112-115