Abstract

Oxidative destruction of polyunsaturated fatty acids of membrane phospholipids, a phenomenon generally termed lipid peroxidation (LPO), is considered to be an important mechanism of toxicity for a wide variety of chemicals. Among these, cadmium (Cd), a pollutant of industrial and environmental importance, induces LPO in various tissues despite its apparent inability to directly generate free radicals under physiological conditions. Consequently, although LPO is not the primary mechanism of Cd toxicity, it represents an early intracellular response of tissues following exposure to Cd compounds. Recently, the authors reported the in vitro specific response to LPO of liver, lung, heart, kidney, testes and brain tissues incubated with various concentrations of CdCl{sub 2}. LPO was assessed by the measurement of thiobarbituric acid reactive substances (TBARS) which include malondialdehyde and lipid hydroperoxydes, and by gaz chromatographic analysis of evolved hydrocarbons, namely ethane and pentane. To compare the results obtained by both methods, they standardized TEP and TBARS values against incubated controls after subtracting endogenous levels of TBARS (time 0 values) because the measurement of endogenous levels of TEP in tissue incubates is not practicable. The objective of the present report is to clarify this concept in order to adequately compare the data obtained frommore » in vitro and in vivo studies. This should permit a better assessment of the relative importance of tissue responses to LPO following exposure to Cd.« less

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