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The post-translationally modified amino acid 3-methylhistidine (3-MEH) is a component of the contractile proteins actin and myosin. The presence of 3-MEH in urine is associated with protein breakdown or nitrogen loss, as reported in laboratory rats (Kim and Lee 1990), dairy cows (Blum and others 1985, Plaizier and others 2000) and dogs under a variety of physiological conditions (Neumann and others 2008). This modified amino acid results from post-translational methylation of histidine in the t-RNA complex, which occurs only in actin and myosin. After proteolysis, it cannot be recycled (Young and Munro 1978), and therefore, it is removed as waste in the urine (Long and others 1975). Thus, there is a strong correlation between 3-MEH urinal levels and the degree of myofibrillar (contractile) protein breakdown in the absence of renal failure (Nagabhushan and Narasingarao 1978).
Muscle wasting and weakness in humans with heart failure characterised by exercise intolerance and reduced survival (Anker and others 1997, Toth and others 1997), is partly due to increased myofibrillar protein degradation (MPD) causing wasting of both muscle mass and function. Therefore, the estimation of MPD under clinical conditions would be beneficial in assessing the degree of heart failure. Although accurate estimations of MPD can be achieved by using isotope methods (Smith and Sugden 1996), this is impractical in a clinical setting. Therefore, MPD levels are usually estimated by either assessing the levels of 3-MEH in plasma (Bachmann and others 1984) or in a 24-hour urine output (Long and others 1981).
The association of plasma 3-MEH levels with systemic diseases has rarely been studied in dogs. Previous studies in dogs with chronic renal failure had a lower clearance of 3-MEH compared with normal dogs (Hansen and others 1992). More recently, it has been reported that the serum concentrations of 3-MEH was significantly increased in …
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