Evaluation of clenbuterol-induced changes in blood biochemical parameters in white mice

Clenbuterol is a bronchodilator which is FDA-approved for treatment chronic obstructive pulmonary disease (COPD) in horse and nonlacting cattle1,2. Clenbuterol binds selectively to β2-receptor in smooth muscles and consequently causing muscle relaxation. The recommended dose of clenbuterol for treatment COPD in veterinary is 0.8μg/kg twice daily1,3. At doses 5-10 folds higher than therapeutic dose, clenbuterol induces weight gain, increases muscle and decreases adipose tissue mass4. Due to its anabolic effects, clenbuterol is illegally used in animal production as a promoting agent and is abused by sportsmen for bodybuilding1,5,6. The chemistry structure of clenbuterol is similar to derivations from endogenous catecholamines. The 3,5-dichloro groups prevent clenbuterol from being metabolized by catecholO-methyltransferase (COMT), which results in its long half-life and its accumulation in animal tissues4. Researches on clenbuterol pharmacokinetics in men and animals reported that clenbuterol was well-absorbed when administered orally and excreted predominantly via urine1,5. After administering orally for 21 consecutive days at dosage of 10-20 times higher than the therapeutic dose, it was observed that clenbuterol accumulated in liver, bile, eye and other edible tissues7. Additionally, clenbuterol residues in animal tissues were found to be unaffected by boiling water and a range of cooking processes such as boiling, frying, roasting5. Consumption of clenbuterol-contaminated food can lead to