Microcystin-LR (MC-LR) has received worldwide concern for its hepatotoxicity with maximum acceptable daily intake of 0.0015 mg/L (1.5 μg/L) [Federal-Provinicial-Territorial-Committee-on-drinking-water-2002]. Comprehensive immunotoxicity data is still deficient with MC-LR. To curb the menace of MC-LR, Quercitin (QE), himalaya made hepatotonic Liv52 were studied. To investigate the immunotoxic properties of MC-LR, QE and Liv52, primary splenocyte cells prepared, cultured, and immunoproliferation assay with mitogens lipopolysaccharide (LPS) or concanavalin A, (Con A) was done for, immunophenotyping, cell cycle and apoptotic studies. In current study, we have divided the splenocytes into 4 groups, i.e., Group I: Normal saline, Group II: MC-LR (0.1 μM), Group III: MC-LR (0.1 μM) + QE (20 μM), and Group IV: MC-LR (0.1 μM) + Liv52 (25 μg/ml) and treated with maximum < CC50 concentration. MC-LR enhanced proliferation of Con A and LPS stirred splenocytes at 24 h, whereas QE and Liv52 both act as antimitogenic. With combined mixture of MC-LR + QE, a significant increase in proliferation compared to mitogen or MC-LR was observed. MC-LR down-regulated expression of CD19+, CD3e+, CD4+, CD8+, (1.05%), (18.9%), (8.9%), and (7.8%) respectively in comparison to Group I. Down-regulation of 10% and 28% is observed in CD19+ and CD4+ populations with MC-LR and QE. The Liv52 addition concealed MC-LR adverse properties in most effective way. MC-LR induced G1-phase significant declined cell cycle arrest at S phase (9.26%) and G2/M phase (26.31%) was observed. QE and Liv52 mask the activity of MC-LR. Further apoptotic study revealed that MC-LR treatment decreases late apoptotic cells compared to control with no significant change in live and early apoptotic cells. Although QE increased live cells and Liv52 significantly increased late apoptotic cells, these results suggest that a <CC50 concentration (0.1 μM) of MC-LR may have immunosuppressive activity. Liv52 is found to be a more potent drug to counteract this cyanotoxin.
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