%0 Journal Article
%T Flow cytometric probing of mitochondrial function in equine peripheral blood mononuclear cells
%A Dominique Cassart
%A Thomas Fett
%A Micha£żl Sarlet
%A Etienne Baise
%A Freddy Coignoul
%A Daniel Desmecht
%J BMC Veterinary Research
%D 2007
%I BioMed Central
%R 10.1186/1746-6148-3-25
%X The JC-1-associated fluorescence orange and green values and their ratio were proved to be stable over time, independent of age and sex and hypersensitive to intoxication with a mitochondrial potential dissipator. Unless time elapsed between blood sampling and laboratory processing does not exceed 5 hours, the values retrieved remain stable. Reference values for clinically normal horses are given.Whenever a quantitative measurement of mitochondrial function in a horse is desired, blood samples should be taken in sodium citrate tubes and kept at room temperature for a maximum of 5 hours before the laboratory procedure detailed here is started. The hope is that this new test may help in confirming, studying and preventing equine myopathies that are currently imputed to mitochondrial dysfunction.Equine atypical myopathy affects horses and ponies kept on pasture and not exercised either prior to or at the time of the first clinical signs. All cases have been reported in the springtime or autumn and after a sudden drop in the minimum daily temperature [1,2]. Affected horses are usually well and suddenly display signs of acute myopathy (stiffness, muscle pain, muscle fasciculations, abnormal gait, recumbency, myoglobinuria, tachycardia, sweating), with no hyperthermia and unchanged appetite [3]. Unlike the other types of myopathy, this condition is often fatal within 12 to 72 hours. Blood analysis consistently shows a spectacular increase in muscle enzymes, in particular the creatine-kinases [3]. Recently, a detailed macroscopical, histopathological, enzymohistochemical and ultrastructural study of 32 clinical cases was reported [2]. The morphopathological picture of the disease suggested a mitochondrial disorder the characteristics of which are compatible with those of equine toxic myopathies due to plant, bacterial or fungal toxins [4-9]. Although morphologic clues of mitochondrial dysfunction in these equine diseases have accumulated, a functional confirmation is still
%U http://www.biomedcentral.com/1746-6148/3/25