Protein damage, as a primary phytotoxic consequence of in vivo lipid peroxidation, induced by the diphenyl ether herbicide oxyfluorfen [2-chloro-1-(3-ethoxy-4-nitrophenoxy)-4-(trifluoromethyl)benzene] at a concentration of 10 μM, was measured with the green alga Scenedesmus acutus. In the light, water-soluble proteins are destroyed by a herbicide-induced peroxidation process that can be detected by production of fluorescent products and loss of specific amino acid residues of proteins. The water-soluble cytochrome c-553 and the membrane-bound cytochrome f-553, components of the photosynthetic electron transport, were specifically used as sensitive markers for protein damage, measured as decrease of redox reactions of the cytochromes. Under peroxidizing conditions, destruction of the algal cytochrome c is significantly higher than destruction of membrane-bound components, such as cytochrome f and chlorophyll. Protection against protein loss is achieved by the nonbiological antioxidant ethoxyquin (1,2-dihydro-6-ethoxy-2,2,4-trimethylquinoline) or the photosynthesis inhibitor diuron [N′-(3,4-dichlorophenyl)-N,N-dimethylurea].

Seeds of wild rice (Zizania palustris var. interior) have been reported to show maximum survival when dehydrated at 25°C. It has also been reported that axis cells sustain least damage at this drying temperature. In the present study, a linear relationship between drying rate and dehydration temperature was established. Whereas the highest positive tetrazolium staining and lowest leakage were recorded for seeds dehydrated at 25°C, maximum germination was recorded for seeds dried at 20°C. A proportion of seeds showed glass formation irrespective of the dehydration temperatures used. Parameters of the glass to liquid transition, however, correlated with neither water content nor sugar profiles. The ratio of raffinose to sucrose was similar in all the treatments. A hydroperoxide test revealed a linear relationship between peroxide levels and drying temperature, although fatty acid amounts were not correlated with hydroperoxide amounts. Butanal amounts and total aldehydes evolved, on the other hand, showed a high negative correlation with peroxide amounts. Electron microscopy showed that the variability and relative abundance of peripheral membrane complexes (PMCs) was highest for embryonic axes dehydrated at 25°C and lowest for cells of embryonic axes of seeds dried at 10°C. Furthermore, intramembrane particles (IMPs) were evenly distributed in cells of axes dried at 25 or 37°C. In contrast, membranes of cells of axes dehydrated at 10°C showed large IMP-free areas. The relative abundance of IMPs was highest in cells of embryonic axes dried at 25°C and lowest in cells of axes dehydrated at 10°C. From these observations, it is suggested that membrane phase transitions, with the concomitant elimination of proteins, accompany dehydration of Z. palustris seeds at 10°C, whereas at 37°C peroxidation may predominate.

Triacylglycerol-rich lipoproteins (TGRLP) were isolated from Cu-deficient and control rats. TGRLP from Cu-deficient rats appeared more fluid than those from controls as sensed by the fluorescence anisotropy of 1,6-diphenyl-l-3,5-hexatriene (DPH). This high fluidity was related to alow cholesterol: phospholipid ratio and high triacylglycerol content in these lipoproteins. TGRLP from Cu-deficient rats were more susceptible to in vitro peroxidation than lipoproteins from control rats as shown by the rate of diene conjugation. The damage induced by the peroxidation resulted in a more ordered state of the lipid fraction especially in lipoproteins from Cu-deficient rats. Thus, after in vitro peroxidation, TGRLP from Cu-deficient rats were more rigid than those from controls. These results suggest that Cu deficiency induces modifications in physicochemical properties of TGRLP which could affect their metabolism.

Given the current interest in the cardiovascular complications of Mg deficiency, the aim of the present experiment was to investigate the effect of Mg deficiency on the time-course of lipoprotein oxidation and to assess whether short-term Mg deficiency results in vitamin E depletion that predisposes lipoproteins and tissues to subsequent oxidation. Weanling rats were pair-fed for 8 d with control and Mg-deficient diets respectively. Plasma triacylglycerol and α-toeopherol levels were significantly greater in Mg-deficient rats compared with control animals. The increase in plasma apolipoprotein B concentration indicated that a corresponding increase in plasma triacylglycerol-rich lipoproteins (TGRLP) occurred in Mg-deficient animals. Hyperlipaemia was associated with modifications in the composition of TGRLP. The proportion of triacylglycerols was elevated whereas that of cholesterol and protein was reduced, and Mg deficiency resulted in a slight significant reduction in α-tocopherol content. When the TGRLP fractions were subjected to in vitro Cu-induced oxidation the lipoprotein fractions from Mg-deficient rats were more susceptible to oxidative damage than lipoprotein fractions from control rats. Mg deficiency did not modify the α-tocopherol content of liver, heart and skeletal muscle. However, after exposure of tissue homogenates to Fe-induced lipid peroxidation, thiobarbituric acid-reactive substances were significantly higher in tissues from Mg-deficient rats compared with those from control rats. These results complement previous findings, showing that Mg deficiency increases the susceptibility of TGRLP and tissues to peroxidation and suggest that oxidative damage is not the result of a decrease in vitamin E antioxidant status.