This is evident from decreased cell viability, decreased ascites volume, and increased best survival time of mice treated daily with LA. In accordance with the present results, it has been shown that LA induces p27Kip1-dependent cell cycle arrest and apoptosis in MCF-7 human breast cancer cells [26]. It is also reported that the proliferation of ovarian epithelial cancer cells was significantly decreased in response to treatment with LA in a dose-dependant manner [10]. Additionally, it is reported that treatment of Jurkat and CCRF-CEM human T lymphoma leukaemic cells with LA led to the dose-dependent inhibition of DNA replication and cell proliferation [25]. Furthermore, it indicated that LA exerts an inhibitory effect on cell proliferation via epidermal growth factor receptors and Akt signal transduction and induces cancer cell apoptosis in MDA-MB-231 human breast cancer cells [27].

Taken together, these findings indicate that LA inhibits the proliferation of a wide variety of cancer cells and tumor promotion in addition to its potential use in the prevention of cancer.EAC-bearing mice showed to be under higher oxidative stress than control animals indicated by elevated lipid and protein oxidation and reduced endogenous antioxidants in the liver. In correlation, it is reported a decrease in SOD activity in EAC-bearing mice which might be due to the loss of MnSOD activity in EAC cells and the loss of mitochondria [28], leading to a decrease in total SOD activity in the liver [29].

Reactive oxygen species (ROS) and other free radicals are believed to be important in tumor promotion and progression and considered the main cause of organ injury and systemic dysfunction Drug_discovery [30, 31]. In the present study, LA was able to control the upsurge in the lipid and protein oxidation in liver via modulation of antioxidants levels in the liver of EAC-bearing mice. LA scavenges the singlet oxygen, and hydrogen peroxide, hydroxyl radicals and also chelates the ferrous ions involved in the production of hydroxyl radicals [3]. Excess ROS can damage hepatocytes and activate hepatic stellate cells [32, 33], which play a central role in liver damage and fibrosis [34]. We found that administration of LA to mice implanted with EAC inhibited the development of liver injury, as indicated by reductions of liver function enzymes.If oxidative stress is involved in the origin of EAC-induced liver oxidative injury, then a successful antioxidant treatment should protect against that injury.