The trifunctional amino acid D-penicillamine (D-P) is commonly used to treat rheumatoid arthritis as well as scleroderma, cystinuria and Wilson’s disease. Adverse reactions are observed in between half and two thirds of subjects undergoing chronic treatment with this agent [I] . The development of a skeletal muscle myopathy is one of the reactions to D-P treatment. However, the pathogenetic mechanisms for D-P induced myopathy are unknown although some auto-immune processes have been described 12-41. We hypothesized that the chelating properties of D-P may be a contributing factor if muscles are indirectly affected by changes in liver or whole body stores of metals To address these issues an animal model was developed in which both therapeutic and high doses of D-P were administered to rats Male Wistar rats were obtained from accredited suppliers and housed in standard conditions until they weighed approximately I 5 0 g body weight. They were then ranked and divided into three groups of equal mean body weight and injected in the post-absorptive state with either saline or D-P. All doses were administered as 1 mlllOO g body weight, ip. The D-P was dissolved in 0.15 moll1 NaCL Rats were starved throughout the study and killed 24 hours after dosage with saline or D-P. The groups were as follows: { 1) Saline (0.15 moll1 NaCI). (2) D-penicillamine, 5 mgllOO g body weight;