UV-A produced a dose-dependent linear increase of peroxidation in linolenic acid micelles as detected by the assay of (i) conjugated dienes, (ii) hydroperoxides, (iii) malondialdehyde (MDA), and (iv) the fluorescent adduct formed by the reaction of MDA with the amino acid, glycine. While sodium formate, dimethyl sulfoxide, superoxide dismutase, and ethylenediamine-tetraacetic acid produced no significant inhibition, some generally used singlet oxygen quenchers, β-carotene, dimethylfuran, L-histidine, and sodium azide, caused significant inhibition of the UV-A-induced peroxidation of the linolenic acid micelles. α-Tocopherol and butylated hydroxytoluene produced more than 90% inhibition of the UV-A-induced peroxidation. ESR spectrometry revealed the formation of 2,2,6,6-tetramethylpiperidine oxide in the UV-A-irradiated aqueous solution of 2,2,6,6-tetramethylpiperidine. The involvement of singlet oxygen <tex-math>$({}^{1}{\rm O}{}_{2})$</tex-math> in the UV-A-induced peroxidation of linolenic acid micelles is discussed.

Ultrasonic radiation produced a dose-dependent linear increase in lipid peroxidation in the liposomal membrane as reflected in the measurements of conjugated dienes, lipid hydroperoxides, and malondialdehydes (MDA). Production of MDA was confirmed by spectrophotometric and spectrofluorometric methods including the detection of excitation (360 nm) and emission (435 nm) maxima characteristic of the MDA-glycine adduct formed after addition of glycine in the system. Ultrasound of frequencies 20 kHz (used for laboratory purposes) and 3.5 MHz (used for clinical purposes) produced MDA in an identical manner. Ultrasound-induced lipid peroxidation was enhanced synergistically by 2.5× 10 2 μM ascorbic acid but inhibited significantly by 10 4 μM ascorbic acid. Ultrasound-induced production of MDA could not be inhibited to any significant degree by superoxide dismutase, histidine, dimethylfuran, or β-carotene but was very significantly inhibited by cholesterol (93%), butylated hydroxytoluene (88%), α-tocopherol (85%), sodium benzoate (80%), dimethyl sulfoxide (80%), sodium formate (64%), and EDTA (64%). The scavenger studies indicated the functional role of ${\rm OH}^{\bullet}$ radicals in the initiation of ultrasound-induced lipid peroxidation.

High-energy α particles produced a dose-dependent linear increase in different lipid peroxidation products (e.g., malondialdehyde (MDA), conjugated dienes, and hydroperoxides) in the dried thin film state. An inverse dose-rate effect was observed when the dose rate was varied by changing either the α-particle fluence rate or the α-particle energy. The antioxidants α-tocopherol and butylated hydroxytoluene (BHT) suppressed the α-particle-induced lipid peroxidation in the dried thin film state, and in this respect α-tocopherol was found superior to BHT. It was found that α-tocopherol was equally efficient in inhibiting lipid peroxidations by α particles and ultraviolet light.

Ultraviolet radiation and sunlight caused lipid peroxidation in the liposomal membrane (as detected by measurement of the oxidation index, <tex-math>$A_{233}/A_{215}$</tex-math>, and the amount of malondialdehyde formed) and made the membrane leaky (as revealed by the release of the trapped chromate anions). The oxidation index and the formation of malondialdehyde increased linearly with increasing dose of radiation and depended significantly on the dose rate. The effects were smaller in liposomes derived from Vibrio cholerae phospholipid than in those derived from egg lecithin. The effects of the radiation dose and dose rate on hemolysis and peroxidation (MDA formation) of the erythrocyte membrane followed a similar pattern. A direct correlation between the percentage leakage of chromate (Y) and the oxidation index (X) of the liposomal system was obtained as Y = 236.5 × X.