It could be either related to bone disease in your control gp or that the treatment causes a significant decrease in serum ALP similar to the case of Ribavirin used for the treatment of chronic hepatitis C and it is known to affect the serum levels of ALP and ALT.
But the drug should result in increase in ALP, as an effect of its hepatotoxic action, on the other hand, I found the result of the control group is higher than the normal ones (for the THIRD time)???
Regarding the animal issue, I'm sure of the elimination of any co-exciting disease that can interfere with the results
It is better to give more explanations about the experiment. What toxin was used? The method of ALP assay? Sample collection method? How much difference among the treatments?
Overall, if you have a valid reference interval for ALP in your tested animal, check if the value of the control group falls within. If yes, you can't say it is higher; if not, you are right. Do same for the ALP values of treated animals. If you had no reference interval and just make comparison among the GROUPS, you should say "the values of treated fish were lower than that of the control animal".
Also, if you are solely believe that the drug should cause ALP activity elevation, you should check the interference in the measurement. You should carefully your sample collection and preservation. Also,should check if the drug resulted in change in the other plasma parameters interfering ALP assay.
Firstly, What about the other liver function enzymes, are there any elevation? Secondly, Did you measure all the tested enzymes at zero time, that’s mean before you starting your experiment? So you got these differences.
Thanks for passing through, regarding your comment, yup, the other biochemical blood parameters are high (ALT, AST...etc), which confirm the hepatotoxicity. Secondly, I didn't measure these enzymes at the zero time, for all the groups I compare it to the negative untreated control group. My problem exactly why the treated groups have a high reduction in ALP level (nearly two fold), while the control group remains high, taking into account that, the drug should elevate the levels of ALP
I think your treated or tested drug, also induced deficiency of one of these vitamins or minerals like zinc, magnesium, phosphorus and/or vitamin C, all these may reflect on the ALP level, I advise you to measure that parameters to be sure about your results.
I think your treated or tested drug, also induced deficiency of one of these vitamins or minerals like zinc, magnesium, phosphorus and/or vitamin C all these may reflect on the ALP level, I advise you to measure that parameters to be sure about your results.
Do you think the theory of deficiency of the vitamins and minerals that you mentioned is also applicable in case of severe reduction of another hepatotoxic parameter like ALT??
Since you treated all animals (control and treated) in a similar way except for drug treatment (i.e. similar diet, similar ration, similar temperature, similar space and ...), thus, dietary deficiency seems not to be the cause of reduction in ALP activity (With respect to dear Doaa).
I suggest you to check if there are any difference among the animal of different groups, rather than drug treatment. e.g. if feed intake (or any other factor rather than drug treatment) was affected by treatment. If such differences are detected, then your measured parameters (enzymes) were not solely affected only by drug treatment.
I understand your point, but it is clear that hepatotoxicity was confirmed by measuring the blood biochemical indicators as I mentioned earlier, and by default, toxicity will results in changing on the all animal behavior (including other factors beside feed intake), and we use the enzyme analysis for confirmation of this toxicity. At the end, I'm searching for a scientific justification on the situation that mentioned in the question. I hope you get my point