Although it has been reported that injections of gentamicin induces li
pid peroxidation in rat renal cortex (Ramsammy et al. (1985) Biochem.
Pharmacol. 34, 3845-3900), our results showed no modification of thiob
arbituric-reagent substances (TEARS) or in analysis of the polyunsatur
ated fatty acid profile. Moreover, endogenous vitamin E and glutathion
e were not consumed. In in vitro systems, gentamicin incubated with mi
crosomes, homogenates and kidney slices from the normal rat failed to
induce lipid peroxidation. We show that the increase in TEARS in vivo
detected by Ramsammy et al. was wrongly attributed to the oxidant powe
r of gentamicin. As this antibiotic does react positively to thiobarbi
turic acid in the presence of a system generating free radicals, it is
possible that these authors accidentally introduced such a system int
o their experiments.