Gentamicin-induced kidney damage and lipid peroxidation in rats.
Although it has been reported that injections of gentamicin induces lipid peroxidation in rat renal cortex (Ramsammy et al. (1985) Biochem. Pharmacol. 34, 3895-3900), our results showed no modification of thiobarbituric-reagent substances (TBARS) or in analysis of the polyunsaturated fatty acid profile. Moreover, endogenous vitamin E and glutathione were not consumed. In in vitro systems, gentamicin incubated with microsomes, homogenates and kidney slices from the normal rat failed to induce lipid peroxidation. We show that the increase in TBARS in vivo detected by Ramsammy et al. was wrongly attributed to the oxidant power of gentamicin. As this antibiotic does react positively to thiobarbituric acid in the presence of a system generating free radicals, it is possible that these authors accidentally introduced such a system into their experiments.
Fauconneau
B
B
Institute of Xenobiotic Studies, Faculty of Pharmacy, Poitiers, France.
Tallineau
C
C
Huguet
F
F
Piriou
A
A
D000818:Animals; D005227:Fatty Acids / Q000378:metabolism; D005839:Gentamicins / Q000633:toxicity*; D066298:In Vitro Techniques; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced*; D015227:Lipid Peroxidation / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014810:Vitamin E / Q000378:metabolism
D005227:Fatty Acids; D005839:Gentamicins; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E