Especially suitable for the specific and very sensitive labeling of cysteine-containing peptides prior to isolation are N-maleimide (DABM), N-(7-dimethylamino-4-methyl-3-coumarinyl)maleimide (DACM), N-(1-pyrenyl)maleimide, and 4-aminosulfonyl-7-fluoro-2,1,3-benzoxdiazol (ABDF).Ĭysteine is readily converted to the corresponding disulfide, cystine, even under mild oxidative conditions, such as treatment with iodine or potassium hexacyanoferrate(III). Johanne Martel-Pelletier, in Rheumatology (Sixth Edition), 2015 Intraarticular injections Stronger oxidation of cysteine, and also of cystine, e.g., with performic acid, yields the corresponding sulfonic acid, cysteic acid. In one of the intraarticular knee injection models OA is induced by mono-iodoacetate (MIA), an inhibitor of glycosis. 35 MIA injection induces alterations in chondrocyte biology in contrast to the mechanical models, in which joint instability is created. This model has been induced mainly in the rat, mouse, and guinea pig. The severity of joint alterations from MIA injection is dose dependent, and MIA generates pain and structural and biochemical alterations associated with OA. There is considerable variation in the dose and volume used in preclinical studies to induce OA in the MIA model (1 to 4.8 mg). In cartilage, the changes are characterized by proteoglycan depletion and degradation in which aggrecanase- and MMP-generated catabolic epitopes have been detected. The cartilage lesions develop rapidly following MIA injection. The classic duration for this model is 28 to 30 days, but it has been studied for up to 56 days. 35 Cartilage surface irregularities are present 7 days after injection, and the lesions reach maximal intensity between 14 and 21 days depending on the dose injected.
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