TABLE 2.

EFFECT OF LPS ON GSH, CySS, CyS TRANSPORT (SYSTEMS)

Thiol/Transport System	Effects	Model	Mechanism	Putative Function	Ref.
GSH/transporter unknown	300% increase in GSH efflux, 15 min after LPS* (5 mg/kg body wt; intravenously)	In vivo, hepatic sinusoids	Increase activity of GSH transporter by LPS-mediated induction of complement	Protect against extracellular oxidant stress	(9)
Cystine/xc−	∼3-fold increase in CySS influx, 6 h after LPS (1 ng/ml)	In vitro, murine primary peritoneal macrophages	Transcriptional upregulation of xCT	Increase cellular GSH	(37)
Cysteine/A, ASC	∼2.7-fold increase in Cys influx 4 h after LPS (7.5mg/kg body wt; intraperitoneally)	Ex vivo, hepatic membrane vesicles	Increase in Vmax of System A and ASC by LPS-mediated induction of cortisol, TNF-α, and cyclooxygenase- derived products	Support gluconeogenesis and synthesis of acute phase proteins	(41)

Definition of abbreviations: ASC, Na⁺-dependent neutral amino acid transporter; CyS, cysteine; CySS, disulfide cysteine; GSH, glutathione; xCT, subunit of the CySS transporter.

^*Salmonella enteritidis LPS.