Pyridoxylamine 2HCl is an advanced glycation end production (AGEs) and lipoxidation end products (ALEs) inhibitor, to protect against diabetes-induced retinal vascular lesions. Pyridoxylamine limits the formation of CML ((carboxymethyl)lysine) and CEL (Nε-(carboxyethyl)lysine) and cross-linking in skin collagen and, ultimately inhibits the development of nephropathy in STZ-diabetic rats. Pyridoxylamine does not appear to function as an antioxidant since it does not prevent lipid peroxidation reactions. At the same time, it does prevent protein modification by products of lipid peroxidation, including inhibiting formation of malondialdehyde and 4-hydroxynonenal adducts on protein in Zucker rats in vivo[1]. UV-Vis spectrophotometry and fluorescence were used to measure PDA (Pyridoxylamine) reactivity for 57 chemicals including anhydrides, aldehydes, and quinones where reaction rates ranged from 116 to 6.2 × 10(-6) M(-1) s(-1) for extreme to weak sensitizers, respectively. No reactivity towards PDA was observed with the thiol-selective sensitizers, non-sensitizers and prohaptens. The PDA rate constants correlated significantly with their respective murine local lymph node assay (LLNA) threshold EC3 values (R(2) = 0.76). The use of PDA serves as a simple, inexpensive amine based method that shows promise as a preliminary screening tool for electrophilic, amine-selective skin sensitizers[2].
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