Hydralazine impairs up-regulation of RAG-2 gene expression and reduces secondary Ig gene rearrangements. Hydralazine subverts B lymphocyte tolerance to self and contributes to generation of pathogenic autoreactivity by disrupting receptor editing. [1] Hydralazine directly scavenges free acrolein, decreasing intracellular acrolein availability and thereby suppressing macromolecular adduction. Hydralazine inhibits cross-linking if adding 30 min after commencing acrolein exposure but is ineffective if added after a 90-min delay. [2] Hydralazine (0.1-10 mM) inhibits both extracellular and intracellular ROS production by inflammatory macrophages, by a ROS-scavenging mechanism probably affecting superoxide radical (O(2)(-))-generation by xanthine oxidase (XO) and nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NADH/NADPH) oxidase. Hydralazine (0.1-10 mM) significantly reduces NO() generation, and this effect is attributable to an inhibition of NOS-2 gene expression and protein synthesis. Hydralazine also effectively blocks COX-2 gene expression which perfectly correlated with a reduction of protein levels and PGE(2) synthesis. [3] Hydralazine protects against not only acrolein-mediated injury, but also compression in guinea pig spinal cord ex vivo. Hydralazine can significantly alleviate acrolein-induced superoxide production, glutathione depletion, mitochondrial dysfunction, loss of membrane integrity, and reduces compound action potential conduction. [4]

Hydralazine affords strong, dose-dependent protection against the increases in plasma marker enzymes but not the hepatic glutathione depletion produced by allyl alcohol in mice. [5]