Asymptomatic patients infected with human immunodeficiency virus
Single dose of 500 mg, 1500 mg, and 4500 mg, p.o., respectively; 14 days later, followed by 500 mg, 1500 mg, and 3000 mg, p.o., three times per day for 28 consecutive days, respectively
Single-dose administration: plasma levels of OTC can be measured at all doses; four-week administration three times daily: increase whole blood GSH at doses of 1500 mg and 3000 mg
500 mg/kg BW, dietary supplementation for 4 consecutive weeks
Decrease AST, necrosis, inflammation, superoxide production, TNF-α and NF-κB; Increase circulating GSH levels to inhibit the activation of Kupffer cells via glycine-gated chloride channel
Acute experiment: 5 μg/mL (LPS) plus 5 mmol/L (OTC), i.p.; Pretreatment: 0.1% drinking water, dietary supplementation for 10 consecutive days before infusion of LPS; Chronic experiment: on days 8, 9, and 10, 5 μg/mL (LPS) plus 5 mmol/L (OTC), i.p., respectively
Acute experiment: prevent the decrease of cellular GSH and the increase of dialysate cell count; Pretreatment: slow the permeability to proteins; Chronic experiment: prevent peritoneal thickening and neovascularization
80 mg/kg BW, i.g., once daily for 3 consecutive days
Decrease the production of ROS, translocation of NF-κB p65 subunit into nucleus, infiltration of macrophages into renal tissue, and expression of ICAM-1, MCP-1, and caspase 3
100 mg/kg BW, 200 mg/kg BW, and 400 mg/kg, i.p., for gastric secretion study; i.g., for antiulcer study
Reduce the acidity and volume of gastric secretion, attenuate the formation of gastric lesion, and protect the gastric mucosa against gastric wall mucus depletion, NP-SH, and MPO via inhibiting neutrophils and replenishing GSH
DEP-induced cerebral microvessel thrombosis in mice
80 mg/kg BW, i.p., 24 h and 1 h ahead intratracheal instillation of DEP
Abolish DEP-induced macrophage and neutrophil influx and the increased TEAC; protect DEP-induced lung inflammation; and reverse the decreased TEAC, shortened bleeding time, and thrombotic effect of DEP in pial cerebral venules through balancing oxidant-antioxidant status
50 mg/kg BW, 100 mg/kg BW, and 150 mg/kg BW, i.v., tail vein injection, 1 h before or after MCAO; 100 mg/kg BW, i.v., tail vein injection, 3 h or 6 h after MCAO
Reduce brain infarct injury and improve behavioral outcomes; increase GSH; decrease superoxides, neuroinflammation and oxidized proteins; and restore Ubqln1 and conjugated protein