The fatty acid distribution of the main lipid fractions: triglycerides (TG), phosphatidylcholine (PCh), phosphatidylethanolamine (PE), and sphingomyelin (Sph) of muscle from 6 patients with progressive muscular dystrophy (p.m.d.), Duchenne, 8 to 12 years old was estimated and compared with normal controls of different age. In view of the results of several authors about varied fatty acid distribution in immature muscle a third group comprising samples of neonatal muscle was studied. 1. The fatty acid pattern of the lipid fractions TG, Sph, and PE from muscle of patients with p.m.d. shows no important variation in comparison to normal controls. In contrast to this the fatty acid distribution in PCh is extremely varied: the percentage of 18:2 is decreased and corrrespondingly the content of 18:1 is increased. In view of the high percentage (nearly 10%) in which linoleic acid is substituted by oleic acid in PCh, effects on the plasma membrane are to be expected. 2. The fatty acid pattern in neonatal muscle shows in narly all positions of the fractions TG, Sph, PE, and PCh a different distribution from normal or dystrophic muscle. In view of the most important variation in dystrophic muscle it must be stated that generally 18:2 is decreased. This deficit was replaced by an increase of all other fatty acids (not only at a substitution by 18:1 as given in p.m.d.). Therefore the diminished content of linoleic acid in PCh of neonatal and dystrophic muscle cannot be interpreted as expression of a corresponding or similar lipid metabolism in both tissues. The results were seen as signs of significant qualitative alterations especially of PCh in p.m.d. They were discussed as proof of our thesis that the basic defect in p.m.d. concerns the specific acylation of PCh with linoleic acid.

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Summary:When the horseradish peroxidase reaction is stopped with acid, the decay of unconverted hydrogen peroxide is responsible for the further oxidation of o-phenylenediamine. This leads to a time-dependent ilattening of the Standard curve in the enzyme immunoassay, after the reaction has been stopped. Addition of reducing agents, such äs sulphite ions, to the stopping solution, prevents the further oxidation of 0-phenylenediamine by completely reducing the remaining hydrogen peroxide. The developed colour is then stabilized. Stabilisierung der Substratreaktion mit o-Phenylendiamin und Wasserstoffperoxid für Meerrettich-Peroxidase im EnzymimmunoassayZusammenfassung: Nach Abbruch der Peroxidasereaktion durch Säurezugabe führt der Zerfall von nicht umgesetztem Wasserstoffperoxid zur weiteren Oxidation von o-Phenylendiamin, was zu einer Abflachung der Standardkurven im Enzymimmunoassay mit zunehmender Zeit nach Reaktionsabbruch führt. Der Zusatz von Reduktionsmitteln wie beispielsweise Sulfitionen zur Stopplösung verhindert durch Reduktion des verbliebenen Wasserstoffperoxids die weitere Oxidation von 0-Phenylendiamin und stabilisiert die entwickelte Farbe. Introduction immunoassays (EIA).A disadvantage of o-phe-0-Phenylenediamine is one of the most frequently nylenediamine, however, is its instability. It is thereused chromogens for the determination of horseradish fore advisable to perform the reaction in the dark peroxidase. Under optimal reaction conditions a de-and to measure the colour intensity of the developed tection limit of about 2 ng/1 horseradish peroxidase 2.2 diamino azobenzene immediately after stopping is observed (1), which enables highly sensitive enzyme the reaction by addition of acid (2).

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