Evidence of lipoperoxidation induced by lactic acid on kidney homogenates

Sawas and Gilbert (Arch. Int. Pharmacodyn. Ther., 276 (1985) 301-312) reported that the commercial solution of haloperidol induces lipoperoxidation of kidney homogenates from Sprague-Dawley rats. However, it would appear that this effect is attributable to the excipient, lactic acid, rather than to haloperidol itself. Lactic acid enhances susceptibility to lipoperoxidation of kidney homogenates in a dose- and time-dependent manner by increasing production of thiobarbituric acid-reactive substances and slightly decreasing polyunsaturated fatty acids such as arachidonic acid and docosahexaenoic acid. This stimulation of lipoperoxidation may be attributed to a mechanism less dependent on enzymatic action than on Fe2+ and Fe3+. Lactic acid may facilitate iron release and formation of iron complexes, factors which increase susceptibility to oxidative stress.