Background: Hepatotoxicity remains an important clinical challenge. Hepatotoxicity
observed in response to toxins and hazardous chemicals may be alleviated by delivery of the
curcumin in silver nanoparticles (AgNPs-curcumin). In this study, we examined the impact of
AgNPs-curcumin in a mouse model of carbon tetrachloride (CCl4)-induced hepatic injury.
Methods: Male C57BL/6 mice were divided into three groups (n=8 per group). Mice in group 1
were treated with vehicle control alone, while mice in Group 2 received a single intraperitoneal
injection of 1 ml/kg CCl4 in liquid paraffin (1:1 v/v). Mice in group 3 were treated with 2.5 mg/kg
AgNPs-curcumin twice per week for three weeks after the CCl4 challenge.
Results: Administration of CCL4 resulted in oxidative dysregulation, including significant
reductions in reduced glutathione and concomitant elevations in the level of malondialdehyde
(MDA). CCL4 challenge also resulted in elevated levels of serum aspartate transaminase (AST)
and alanine transaminase (ALT); these findings were associated with the destruction of hepatic
tissues. Treatment with AgNPs-curcumin prevented oxidative imbalance, hepatic dysfunction, and
tissue destruction. A comet assay revealed that the CCl4 challenge resulted in significant DNA
damage as documented by a 70% increase in nuclear DNA tail-length; treatment with AgNPscurcumin
inhibited the CCL4-mediated increase in nuclear DNA tail-length by 34%.
Conclusion: Administration of AgNPs-curcumin resulted in significant anti-oxidant activity in
vivo. This agent has the potential to prevent hepatic tissue destruction and DNA damage that
results from direct exposure to CCL4.