Carbon tetrachloride: a hepatotoxin causes oxidative stress in murine peritoneal macrophage and peripheral blood lymphocyte cells.

CONTEXT

Carbon tetrachloride (CCl₄) is frequently used as a chemical inducer of tissue damage. Their effects on mouse peritoneal macrophages and also in peripheral blood lymphocytes are still unknown.

OBJECTIVE

Therefore we tried to focus on intracellular oxidative stress produced by CCl₄ in mouse macrophage and lymphocyte cells.

METHODS

Intraperitoneal administration of CCl₄ induces intracellular superoxide anions production in mouse macrophages and peripheral blood lymphocytes and leads a subsequent lipid peroxidation and protein oxidation. N-acetyl cystein (NAC) and vitamin C were administered intraperitoneally at a dose of 150 mg/kg and their effect on demodulating the oxidative stress is also checked.

RESULT AND DISCUSSION

Several in vitro approaches have already been established as a free radical scavenging models, but this free radical screening models is not always correlated with the in vivo screening models. NAC and vitamin C were administered intraperitoneally and significant reduction of the oxidative stress in term of scavenging of toxic superoxide anion observed in both the macrophages and lymphocytes.

CONCLUSION

Therefore we are hopeful that our work will light a new insight into the screening of in vivo free radical scavenging model for evaluating anti-inflammatory compounds.