S. N. Chatterjee

Liposomes as membrane model for study of lipid peroxidation.

This article describes the properties, production and characterization of liposomes with special reference to their use as membrane model for the study of lipid peroxidation. It presents briefly the methods that can be used for the assay of liposomal lipid peroxidation and brings out the special advantages these liposomes provide in elucidating the mechanism of lipid peroxidation by different physical and chemical agents. Studies involving liposomal lipid peroxidation by different agents and the consequent changes in the structure and function of liposomal membrane have been reviewed briefly.

Estimation of hydroxyl free radicals produced by ultrasound in Fricke solution used as a chemical dosimeter

Abstract Hydroxyl free radicals produced in Fricke solution exposed to 80 kV X-rays or 23 kHz ultrasound (intensity 3 W cm−2) or 20 kHz ultrasound (intensity 18.9 W cm−2) or 3.5 MHz clinical ultrasound (intensity 1.47 W cm−2), as estimated from the Fricke dosimetric data, exhibited a linear dose-response relationship. The dosimeter was found to be effective in the concentration range 1.0–8.0 mM of FeSO4 solution. The hydroxyl radicals produced in Fricke solution were inhibited by the OH radical scavengers dimethyl sulfoxide (200 mM), l -histidine (10 mM) and sodium benzoate (10 mM) in a manner proportional to the rate constants of their reaction with the OH radicals. The power threshold for OH radical formation, which is presumably the threshold for cavity formation, was estimated for 23 kHz ultrasound by this dosimeter as 1.28 W cm−2 for a 4 cm3 sample volume.

The induction of lipid peroxidation in liposomal membrane by ultrasound and the role of hydroxyl radicals

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 X 10(2) microM ascorbic acid but inhibited significantly by 10(4) microM ascorbic acid. Ultrasound-induced production of MDA could not be inhibited to any significant degree by superoxide dismutase, histidine, dimethylfuran, or beta-carotene but was very significantly inhibited by cholesterol (93%), butylated hydroxytoluene (88%), alpha-tocopherol (85%), sodium benzoate (80%), dimethyl sulfoxide (80%), sodium formate (64%), and EDTA (64%). The scavenger studies indicated the functional role of OH radicals in the initiation of ultrasound-induced lipid peroxidation.

UV-A induced lipid peroxidation in liposomal membrane

SummaryUV-A (365 nm) produced a dose-dependent linear increase of lipid peroxidation, as detected by the assay of malondialdehyde (MDA). MDA formation was inversely related to the UV-A dose rate. Sodium formate and ethylenediaminetetra acetic acid (EDTA) could not inhibit by any significant degree the UV-A induced MDA formation. While butylated hydroxy toluene (BHT) caused about 85% inhibition, sodium azide andl-histidine produced 45–50% inhibition of MDA formation. The involvement of singlet oxygen (1O2) in the UV-A induced lipid peroxidation is discussed.

Correlation between UVA-induced changes in microviscosity, permeability and malondialdehyde formation in liposomal membrane.

The lipid peroxidation, 14C-glucose leakage and microviscosity of liposomal membrane increased linearly with increasing UVA fluence. A positive and highly significant correlation was found between these properties of the UVA-exposed liposomal membrane. The possible involvement of singlet oxygen in the UVA-induced damage of liposomal membrane is discussed.

Ultrasonic radiation induced lipid peroxidation in liposomal membrane

SummaryUltrasonic radiation produced a dose dependent linear increase in lipid peroxidation (MDA formation) in the liposomal membrane. The yield of MDA was significantly inhibited by butylated hydroxytoluene (BHT), the antioxidant, sodium formate, the OH⋅ radical scavenger, and EDTA, the metal ion chelator. Ascorbic acid at low concentration increased the ultrasonic induced MDA formation while high concentrations inhibited lipid peroxidation. A mechanism of ultrasound induced lipid peroxidation is suggested.

UVA-induced peroxidation of lipid in the dried film state

Exposure of a dried lipid thin film to UVA produced a dose-dependent linear increase in the three peroxidation products, conjugated diene, lipid hydroperoxide and malondialdehyde (MDA). All three lipid peroxidation products exhibited an inverse dose rate effect. Identical amounts of malondialdehyde were produced when the lipid film was exposed to UVA either directly or through the thickness of the Corning glass on which the film was cast. Antioxidants, alpha-tocopherol, butylated hydroxytoluene (BHT) and the singlet oxygen quencher beta-carotene significantly inhibited the UVA-induced peroxidation of the lipid film. The biological implications of the UVA-induced peroxidation of the dried lipid film are discussed.

Membrane lipid peroxidation by ultrasound: Mechanism and implications

Ultrasonic radiation produced a dose-dependent linear increase in lipid peroxidation in the liposomes membrane as reflected in the measurement of conjugated dienes, lipid hydroperoxides and malondialdehydes. Ultrasound induced malondialdehyde production could not be inhibited by any significant degree by superoxide dismutase or histidine or dimethyl furan but was very significantly inhibited by butylated hydroxytoluene, cholesterol, sodium benzoate, dimethyl sulphoxide, sodium formate and EDTA. The scavenger studies indicated the functional role of hydroxyl radicals in the initiation of ultrasound induced lipid peroxidation.

Lipid peroxidation by ultraviolet light and high energyα particles from a cyclotron

SummaryHigh energyα-particles (∼ 16 MeV) and 254 nm ultraviolet light produced dose dependent linear increase of lipid hydroperoxides in the dried thin film state. For both types of radiation, an inverse dose-rate effect, i.e., a protracted radiation dose was more effective than a shorter, more intense one of larger size, was observed. Ultraviolet light (254 nm) produced higher yields of hydroperoxides in the aqueous liposomal suspension of lipid than in its dried thin film state.

Peroxidation of the Dried Thin Film of Lipid by High-Energy Alpha Particles from a Cyclotron

High-energy alpha 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 alpha-particle fluence rate or the alpha-particle energy. The antioxidants alpha-tocopherol and butylated hydroxytoluene (BHT) suppressed the alpha-particle-induced lipid peroxidation in the dried thin film state, and in this respect alpha-tocopherol was found superior to BHT. It was found that alpha-tocopherol was equally efficient in inhibiting lipid peroxidations by alpha particles and ultraviolet light.