Since AST and ALT are released from damaged liver, these two markers can represent the degree of liver related diseases. However, because these two enzymes are produced from liver, in higher degree of some diseases, hepatocytes can even lose the ability to produce ASL or ALT(hepatocytes may totally die). Briefly, it is possible to observe this phenomenon in clinic.

I think in this situation everything is much simpler. Since the main target organ of cyclophosphamide is the immune system, within reasonable doses the liver is not so heavily loaded, and its metabolism proceeds through the cytochrome p450 system with the formation of not the most toxic metabolites. Given that a human has an average elimination half-life of 3-10 hours, so in mice it will be many times faster. That is why, after 2 hours, the activity of hepatic transaminases remains elevated, and after 6 hours, they normalize.

Hello Lo and Vladimir Lo Tzu Yu Vladimir Shipelin

Thank you so much for the responses. I agree with that, however I have also added PARP inhibitors to the experiment, including Olaparib and DIQ and they remain strong in ALT levels, in fact even higher than cyclophosphamide and acetaminophen, which I later assessed in another experiment. I went on to test all 4 agents for 18 hours, before collecting the serum and noted somewhat elevated levels (40 U/L) for both Olaparib and DIQ (both administered below 10 mg/kg per mouse) and comparatively low levels or APAP and cyclophosphamide (200+ mg/kg per mouse). Any ideas why this might be the case? Thanks,

Sheba