L-Lactic acid ((S)-2-Hydroxypropanoic acid) is a natural product produced by the anaerobic glycolysis of pyruvic acid. L-Lactic acid is a sensitive indicator of tissue hypoxia and can be used as a hemodynamic indicator in critically ill patients.

METHODS: Mouse CD4+CD25-T cells were treated with low-glucose medium containing L-Lactic acid (5-20 mM), and Teff proliferation was detected by Flow cytometry.
RESULTS: L-Lactic acid had a sustained inhibitory effect on T cell proliferation, and apoptosis-independent effect. [1]
METHODS: T cells were cultured in medium containing L-Lactic acid (20 mM), and ROS levels were measured using ROS and superoxide detection assay kits.
RESULTS: A significant reduction in ROS and O2- production was observed in L-Lactic acid-treated T cells. [2]

METHODS: To study its effect on swimming endurance, L-Lactic acid (25-50 mg/kg in 0.9% NaCl) was administered intraperitoneally to ICR mice.
RESULTS: L-Lactic acid enhanced the swimming endurance of mice, and the effect was dose-dependent. [3]
METHODS: To investigate the effect on endotoxemia, L-Lactic acid (80 mg/kg) was intraperitoneally injected into mice, and 20 h later, a lethal dose of LPS (25 mg/kg) was intraperitoneally injected into mice to induce infectious shock.
RESULTS: L-Lactic acid significantly inhibited LPS-induced cytokine induction in mice following endotoxemia.L-Lactic acid treatment decreased glucose uptake and lactate output during LPS stimulation. [4]