• The Plant Pathology Journal
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• v.17 no.1
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• pp.36-39
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• 2001

The secondary effects of pencycuron on cell membrane of Rhizoctonia solani AG4 were investigated by the observation of giant protoplast formation and lipid peroxidation. Compared to protoplasts of R. solani R-C (sensitive strain) and Rh-131 (non-sensitive strain) increased in their size by 2.0-3.5 times 12 h after incubation in potato-dextrose broth containing novozyme (7 mg/$m\ell$) and $\beta$-glucuronidase ($60\mu\textrm{g}/$\textrm{ml}) with 0.6 M mannitol (pH 5.2). The increase of protoplast size in R-C was slightly inhibited from $13.8\textrm{mg}/\textrm{ml}$ without pencycuron to 10.3 ${\mu}{\textrm}{m}$ with 1.0$\mu\textrm{g}$/$m\ell$ of pencycuron. However, the size of giant protoplast of Rh-131 was not affected by the pencycuron treatment. Both strains R-C and Rh-131 did not exhibit the lipid peroxidation 12 h after the application of 1.0 $\mu\textrm{g}$/$m\ell$ pencycuron. The remarkable peroxidation of membrane lipid was observed only in R-C 24 h after pencycuron application, but not in Rh-131. Althought the inhibition of giant protoplast formation and the membrane lipid peroxidation were observed only in the sensitive strain R-C by pencycuron, it is difficult to conclude that these are the primary mechanism of pencycuron. The mild activity of pencycuron on the inhibition of giant protoplast formation and late membrane lipid peroxidation in the fungicide-sensitive strain did not noincid with the dramatic activity of pencycuron in R. solani. Therefore, our results suggest that inhibition of giant protoplast formation and membrane lipid peroxidation is the secondary effect of pencycuron.

• Journal of Nutrition and Health
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• v.25 no.7
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• pp.586-596
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• 1992

To investigate the role of vitamin E in protection against lipid per-oxide formation and to monitor the changes in the status of vitamin E. A and reduced glutathione(GSH) in fish oil feeding male Sprague-Dawley rats were divided into four groups. Control group was fed soybean oil and fish oil groups(FO, FI, FII) fed menhaden oil and soybean oil(9:1) mixture at the level of 10% (w/w) respectively. Dietary vitamin E levels were 30 T, E for control and FI, 2 T.E. for FO and 140 T. E for FII Feeding periods were 4, 8, and 16 weeks. Throughout all periods plasma vitamin E levels(either per ml or per mg lipid) of FO group were extremely low and liver and adipose tissue vitamin E levels were also the lowest among four groups, Plasma vitamin E levels per ml were lower in FI and FII than control but per mg lipid were in the order of FII>FI$\geq$control but vitamin E level per mg lipid did not differ in liver and adipose tissue. As feeding prolonged vitamin E levels in plasma and other tissue were decreased in FO but increased in the other groups. Plsama and liver thiobarbituric acid-reactive substance(TBARS) values were elevated in FO. but increased in the other groups. Plasma and liver thiobarbituric acid-reactive substance(TBARS) values were elevated in FO. While plasma TBARS values as per ml plasma were similar or lower in FI and FII as compared to control plasma TBARS values as per mg lipd and liver TBARS values were in the order of $FI\geqFII>control.$ Plasma and liver vitamin A blood GSH but not liver GSH appeared to be in the order of FII control>FI>FO and this was most significant in 8 weeks. This results suggests that both type of dietary oil and levels of vitamin E affect not only lipid peroxidation but also the status of other physiological antioxidants which have the potential to spare the role of vitamin E.