Effects of soyasaponins on lipid peroxidation through the secretion of thyroid hormones.

We investigated how soyasaponins (SS), which had been isolated from soybeans (Glycine max Merrill, seeds), influenced lipid peroxidation. The in vivo reduction in hepatic lipid peroxidation in mice intraperitoneally injected with total soyasaponins (TSS) was comparable to that which has been observed for alpha-tocopherol (VE). However, TSS and its five main constituent saponins (I, II, III, A1, and A2) had a much weaker in vitro inhibitory effect on lipid peroxidation induced by NADPH in mouse liver microsomes than VE. Therefore, we were not able to explain the in vivo effect of SS on lipid peroxidation level through direct antioxidative effects. We also demonstrated that TSS increased the levels of serum thyroid hormones. The effect of serum thyroid hormones on in vitro lipid peroxidation was much stronger than that observed for VE. Furthermore, the effects of TSS on levels of serum thyroid hormones and LPO were markedly decreased by propylthiouracil, an antithyroid drug. These results indicate that the effects of SS on lipid peroxidation levels appear to be mediated through the secretion of thyroid hormones.

Role of nitric oxide synthase activity in experimental ischemic acute renal failure in rats.

To determine the role of nitric oxide (NO) in acute renal failure (ARF), we have studied the time course change activities to activity of nitric oxide synthase (NOS) isoform activities, both calcium dependent and independent NOS, in experimental ischemic ARF. We have also analyzed change activities to activity of the NOS activities in both renal cortex and medulla. Male SD rats (n = 5) were inducted to ARF by ischemia-reperfusion injury and divided into the following groups; Control group (sham operation), Day 0 group, (measurement performed on that day of operation), Day 1 group, (measurement performed one day after induction of ARF), Day 3 group and Day 7 group. Measurement of NOS activity was based on the following principles; NO is synthesized from arginine by nitric oxide synthase (NOS) and NO is converted to NO2(-)/NO3(-)(NOx) by oxidation. Detection of the final metabolite of NO, NOx was done using flow injection method (Griess reaction). The results were, (1) calcium dependent NOS activity in the cortex and medulla decreased, however it increased in the recovery period in the renal cortex (Cortex; Control, 0.941 +/- 0.765, D0, 0.382 +/- 0.271, D1, 0.118 +/- 0.353, D3, 2.030 +/- 0.235, D7, 3.588 +/- 2.706, Medulla; Control, 1.469 +/- 0.531, D0, 0.766 +/- 0.156, D1, 0.828 +/- 0.187, D3, 2.078 +/- 0.094, D7, 1.289 +/- 0.313 micromol NOx produced/mg protein/30 min). (2) On the other hand, iNOS activity increased in the early phase of ARF, both in the cortex and medulla, but returned to control values during the recovery phase in cortex and was maintained at higher levels in the medulla (Cortex; Control, 0.333 +/- 0.250, D0, 0.583 +/- 0.428, D1, 1.167 +/- 0.262, D3, 0.250 +/- 0.077, D7, 0.452 +/- 0.292, Medulla; Control, 0.139 +/- 0.169, D0, 0.279 +/- 0.070, D1, 1.140 +/- 0.226, D3, 0.452 +/- 0.048, D7, 0.625 +/- 0.048 micromol NOx produced/mg protein/30 min). These findings suggest that the role of NOS in ARF are different for the different NOS isoforms and have anatomic heterogeneity.