Summary Activities of glutamate dehydrogenase and glutamine synthetase were determined using crude extracts of roots and shoots of mycorrhizal and non‐mycorrhizal plants of Trifolium subterraneum L. and Allium cepa L., grown at different levels of fertilizer phosphate. Glutamate dehydrogenase activity was low in all tissues [0.1 to 1.6 μmol NAD(P)H oxidized min−1 gFW−1 tissue] and there was no consistent effect of mycorrhizal infection or phosphate nutrition on this activity. Glutamine synthetase (GS) activity (assayed by the transferase method) was in the range 1 to 40/iimol γ‐glutamyl hydroxamate produced min−1 gFW−1. In general, activity of this enzyme was low in phosphate‐deficient plants and was increased both by mycorrhizal infection and by improved phosphate supply. In T. subterraneum routine assays of GS were done on roots only. The effects of mycorrhizal infection in increasing enzyme activity in roots were similar whether natural soil inoculum (containing a mixture of several mycorrhizal fungi) or inoculum of Glomus mosseae Nichol. & Gerd. was used. Both increased phosphate supply and mycorrhizal infection increased nodulation of clover plants as well as GS activity, so that it was difficult to relate changes in GS activity to the interacting effects of mycorrhizal infection and phosphate nutrition. Onions had low GS activity in uninfected roots, compared with shoots. Again improved phosphate supply resulted in increased enzyme activity in both roots and shoots. However, the patterns of interaction between phosphate supply, P concentration in tissues, mycorrhizal infection and enzyme activity were different in the two tissues. In shoots, as expected, the effects were consistent with an indirect effect of mycorrhizal infection on enzyme activity, via improved P nutrition. In roots there appeared to be a ‘fungal effect’ superimposed on the phosphate effect. This was investigated by manipulating the amount of fungal tissue in mycorrhizal roots via differences in propagule density of G. mosseae in soil. Results were again consistent with the hypothesis that the mycorrhizal fungi contributed GS activity to the symbiotic root system. Fungal structures were separated from roots following digestion in cellulase and pectinase. GS activity was high in fungal tissue from young roots (29 to 31 d), but low in older infections (55 d). The high activity could not have been caused by contamination of fungal tissue by root cells. The digestion technique reduced GS activity in uninfected and infected root segments, so that results obtained with separated fungi are not quantitatively comparable with those obtained from extracts of fresh tissues. We conclude that vesicular‐arbuscular mycorrhizal fungi are able to assimilate ammonium via GS. This ability would be important in increased uptake of nitrogen which is an inevitable prerequisite for increased growth following relief of phosphate stress. It is also consistent with the recent findings by others that hyphae of G. mosseae can absorb and translocate 15NH+4
SUMMARYGrowth and rates of uptake of nitrogen and phosphorus (inflow) in Allium cepa L. were measured in three experiments. EfTects of mycorrhizal infection {Glomus mosseae (Nicol. and Gerd.) Gerdemann and Trappe) and N and P fertilization were investigated. The experiments were carried out in a naturally-lit glasshouse, so that seasonal variations in solar radiation infiuenced experimental results.In all experiments, a large positive growth response to mycorrhizal infection was observed when soil P was low. However, at high soil P smaller growth responses to infection were observed, as expected. Infection was associated with increased inflow of P, at all levels of soil P, even when non-mycorrhizal plants grew as well as or better than mycorrhizal plants. Lower P inflow was observed when infection was low and also at low irradiance in hoth mycorrhizal and non-mycorrhizal plants. The results show that mycorrhizal fungi increase the rate at which P is absorbed from soil, even under conditions which precluded a positive growth response to infection.In plants grown in spring and summer (two experiments), mycorrhizal infection was also associated with increased N inflow. N inflows in both mycorrhizal and non-mycorrhizal plants were lower in a third experiment in late winter and mycorrhizal infection had little or no effect on N inflow in this experiment. Increased N supply increased the inflow of N, concentrations of N in plant tissues and plant growth except in plants that were severely P limited, and there was no evidence that mycorrhizal infection alleviated N stress in low N plants.The results are discussed in relation to the environmental factors limiting plant growth, in particular nutrient uptake via and carbohydrate use by the fungal symbiont.
Cardiac mitochondrial oxidative stress causes mitochondrial damage that plays an important role in the pathology of myocardial infarction. The preventive effects of diosmin on cardiac mitochondrial oxidative stress in isoproterenol-induced myocardial infarcted rats were evaluated. Rats were pretreated with diosmin (10 mg/kg body weight) daily for 10 days. Myocardial infarction was induced in rats by isoproterenol (100 mg/kg body weight) injection twice at an interval of 24 h (on 11th and 12th day). Isoproterenol-induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium ion, and a significant decrease in the levels of heart mitochondrial glutathione peroxidase, reduced glutathione, glutathione-S-transferase, isocitrate, malate, α-ketoglutarate, and succinate dehydrogenases. Transmission electron microscopic findings revealed damaged mitochondria with loss of cristae, swelling, and vacuolation in isoproterenol-induced rats' heart. Diosmin pretreatment showed significant preventive effects on all the biochemical parameters, and the structure of mitochondria was evaluated. Furthermore, the transmission electron microscopic study confirms the biochemical findings. The antioxidant and negative inotropic effects of diosmin inhibited cardiac mitochondrial oxidative stress and prevented mitochondrial damage in myocardial infarcted rats.
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