Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2001-7-25
pubmed:abstractText
Reports in the literature indicate that the trifunctional amino acid D-penicillamine (D-P) induces a variety of muscle abnormalities, although the mechanisms are unknown. We hypothesised that defects may also arise due to the effects of D-P on rates of protein synthesis, possibly via changes in muscle metal composition. Male Wistar rats were injected with D-P at doses of 50 and 500 mg/kg body weight, i.p. Rats designated as controls were injected with 0.15 mol/l NaCl. After 24 h, there were reductions in muscle protein contents, protein synthetic capacities (RNA:protein ratio), fractional rates of protein synthesis, synthesis rates per unit RNA and synthesis rates per unit DNA in skeletal muscles of D-P treated rats. There were no statistically significant differences between the responses of the muscles containing a predominance of either Type I (represented by the soleus) or Type II (represented by the plantaris) fibres. In general, intracellular amino acids were not significantly affected by D-P treatment. Changes in muscle metals included significant reductions in copper, iron and manganese, without alterations in zinc or magnesium. In liver D-P reduced copper and iron though zinc, manganese and magnesium were unaffected. These effects of D-P on muscle may have been direct, as plasma indices of liver (activities of alkaline phosphatase and alanine aminotransferase) and kidney (urea, creatinine and electrolytes) damage were not significantly altered by D-P treatment. Plasma levels of corticosterone, insulin and free T3 were also not significantly affected by D-P treatment. Muscle protein carbonyl concentrations, an index of free radical activity, were similarly unaffected. This is the first report of reduced rates of muscle protein synthesis in D-P treatment. Our data suggests that the reduced rates of muscle protein synthesis may contribute to, or reflect, the muscle abnormalities observed in patients undergoing D-P treatment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1357-2725
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1013-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11470234-Animals, pubmed-meshheading:11470234-Antirheumatic Agents, pubmed-meshheading:11470234-Copper, pubmed-meshheading:11470234-Injections, Intraperitoneal, pubmed-meshheading:11470234-Iron, pubmed-meshheading:11470234-Kinetics, pubmed-meshheading:11470234-Liver, pubmed-meshheading:11470234-Male, pubmed-meshheading:11470234-Manganese, pubmed-meshheading:11470234-Muscle, Skeletal, pubmed-meshheading:11470234-Muscle Fibers, Fast-Twitch, pubmed-meshheading:11470234-Muscle Fibers, Slow-Twitch, pubmed-meshheading:11470234-Muscle Proteins, pubmed-meshheading:11470234-Organ Size, pubmed-meshheading:11470234-Penicillamine, pubmed-meshheading:11470234-Rats, pubmed-meshheading:11470234-Rats, Wistar, pubmed-meshheading:11470234-Spectrophotometry, Atomic, pubmed-meshheading:11470234-Time Factors, pubmed-meshheading:11470234-Zinc
pubmed:year
2001
pubmed:articleTitle
Skeletal muscle protein loss due to D-penicillamine results from reduced protein synthesis.
pubmed:affiliation
Molecular and Cellular Protein Biochemistry Laboratory, Department of Nutrition and Dietetics, King's College London 150 Stamford Street, SE1 9NN, London, UK. victor.preedy@kcl.ac.uk
pubmed:publicationType
Journal Article, Comparative Study