Comparing the effects of treatment with ammonium molybdate versus ammonium molybdate and phenoxy-2-methyl-2-propionic acid on liver functions in natural copper poisoning of sheep

Abstract

Aim of the presented study is to compare the effects of treatment with ammonium molybdate versus ammonium molybdate and phenoxy-2-methyl-2-propionic acid on liver functions in natural copper poisoning of sheep and overall treatment responses in sheep naturally poisoned with copper (Cu). Study was conducted on 80 yearlings aging between 6-9 months. AM + PMPA group (n =50) received ammonium molybdate and PMPA and AM group (n =30) received only ammonium molybdate. First blood samples were collected before the treatments. PMPA was administered once daily intramuscularly at dose of 10 mg/kg for the first three days of the study to AM + PMPA group. AM + PMPA and AM groups both received ammonium molybdate two times with one week interval at dose of 1.34 mg/kg (1 cc per 10 kg BW, of %1.34 ammonium molybdate in saline solution) subcutaneously. Second blood samples were collected from all 80 animals on day 21 of the study. Cu levels were measured in a subgroup of randomly selected 9 (5 from AM + PMPA and 4 from AM group) animals on days 0 and 21 of the study. Mean Cu levels were 158.25 +/- 14 mu g/dl and 156.75 +/- 9 mu g/dlon day 0 and 129 +/- 9 mu g/dl and 154.5 +/- 22 mu g/dl in AM + PMPA and AM group respectively. AST levels decreased from 502 +/- 67.2114 to 168 +/- 10.1 IU/L in AM + PMPA group (P < 0.001) and from 423 +/- 71.1 IU/Lto 202 +/- 17.1 IU/L in AM group (P = 0.005) on day 21 of the study. GGT levels were 250 +/- 24.2 IU/L and 248 +/- 28.1 IU/L on day 0 and decreased to 160 +/- 16.41 U/L and 166 +/- 22.2 IU/L on day 21 in AM + PMPA and AM group with significance of P=0.001 and P=0.037 respectively. Two animals from AM group and one from AM + PMPA group died during the study period. Based on the more pronounced decrease in AST and GGT levels in AM + PMPA group we conclude that PMPA has beneficial effects on liver functions in chronic copper poisoning of sheep probably as a result of decreased lipid peroxidation in hepatocytes and/or increased Cu elimination by cholerectic effects of PMPA.