To elucidate the protective effects of glutathione against iron-induced peroxidative injury, changes in the hepatic glutathione metabolism were studied in chronically iron-loaded mice. When the diets of the mice were supplemented with carbonyl iron, iron deposition occurred primarily in the parenchymal cells of the liver. In addition, expiratory ethane production was elevated, suggesting an enhancement in lipid peroxidation. In iron-loaded mice, the total hepatic glutathione contents were higher (6.21 +/- 0.53 mumol/g wet wt.) than in control mice (4.61 +/- 0.31 mumol/g wet wt.), primarily due to an increase in the reduced glutathione contents. The value of oxidized glutathione was also higher (98.5 +/- 8.1 nmol/g wet wt.) than in the controls (60.8 +/- 9.5 nmol/g wet wt.), and the ratio of oxidized glutathione to total glutathione increased. The excretion rate of glutathione from the hepatocytes in iron-loaded mice also increased. These observations suggest that chronic iron-loading of mice stimulates lipid peroxidation and oxidation of glutathione and that peroxidized molecules may be catabolized using reduced glutathione. 相似文献
A thermotolerant bacterium, identified as Bacillus licheniformis, completely utilized 0.1% (w/v) NH4NO3 at 30 and 50°C under aerobic condition. The addition of 0.5 mM Fe2+ to the NH4NO3 medium markedly promoted the utilization of NH4+ and NO3−. At 50°C, of total nitrogen originally provided, 24% was taken up into the cells and 20% remained in the culture supernatant.
Residual nitrogen (56%) was probably removed into the atmosphere. The cell extracts contained enzymes involved in denitrification.
GC-MS demonstrated that NH4 15NO3 had been converted to 15N2O. These results indicate that the strain has denitrification ability under aerobic condition. 相似文献
Oxidative stress plays an important role in the structural and functional abnormalities of diabetic heart. Glutathione peroxidase (GSHPx) is a critical antioxidant enzyme that removes H(2)O(2) in both the cytosol and mitochondia. We hypothesized that the overexpression of GSHPx gene could attenuate left ventricular (LV) remodeling in diabetes mellitus (DM). We induced DM by injection of streptozotocin (160 mg/kg ip) in male GSHPx transgenic mice (TG+DM) and nontransgenic wildtype littermates (WT+DM). GSHPx activity was higher in the hearts of TG mice compared with WT mice, with no significant changes in other antioxidant enzymes. LV thiobarbituric acid-reactive substances measured in TG+DM at 8 wk were significantly lower than those in WT+DM (58 +/- 3 vs. 71 +/- 5 nmol/g, P < 0.05). Heart rate and aortic blood pressure were comparable between groups. Systolic function was preserved normal in WT+DM and TG+DM mice. In contrast, diastolic function was impaired in WT+DM and was improved in TG+DM as assessed by the deceleration time of peak velocity of transmitral diastolic flow and the time needed for relaxation of 50% maximal LV pressure to baseline value (tau; 13.5 +/- 1.2 vs. 8.9 +/- 0.7 ms, P < 0.01). The TG+DM values were comparable with those of WT+Control (tau; 7.8 +/- 0.2 ms). Improvement of LV diastolic function was accompanied by the attenuation of myocyte hypertrophy, interstitial fibrosis, and apoptosis. Overexpression of GSHPx gene ameliorated LV remodeling and diastolic dysfunction in DM. Therapies designed to interfere with oxidative stress might be beneficial to prevent cardiac abnormalities in DM. 相似文献
Although recent studies suggest that hyperlipidemia is a risk factor for osteoarthritis
(OA), the link between OA and hyperlipidemia is not fully understood. As the number of
activated, circulating myeloid cells is increased during hyperlipidemia, we speculate that
myeloid cells contribute to the pathology of OA. Here, we characterized myeloid cells in
STR/Ort mice, a murine osteoarthritis model, under hyperlipidemic conditions. Ratios of
myeloid cells in bone marrow, the spleen, and peripheral blood were determined by flow
cytometry. To examine the influence of the hematopoietic environment, including abnormal
stem cells, on the hematopoietic profile of STR/Ort mice, bone marrow transplantations
were performed. The relationship between hyperlipidemia and abnormal hematopoiesis was
examined by evaluating biochemical parameters and spleen weight of F2 animals
(STR/Ort x C57BL/6J). In STR/Ort mice, the ratio of CD11b+Gr1+ cells
in spleens and peripheral blood was increased, and CD11b+Gr1+ cells
were also present in synovial tissue. Splenomegaly was observed and correlated with the
ratio of CD11b+Gr1+ cells. When bone marrow from GFP-expressing mice
was transplanted into STR/Ort mice, no difference in the percentage of
CD11b+Gr1+ cells was observed between transplanted and age-matched
STR/Ort mice. Analysis of biochemical parameters in F2 mice showed that spleen
weight correlated with serum total cholesterol. These results suggest that the increase in
circulating and splenic CD11b+Gr1+ cells in STR/Ort mice originates
from hypercholesterolemia. Further investigation of the function of
CD11b+Gr1+ cells in synovial tissue may reveal the pathology of OA
in STR/Ort mice. 相似文献
Two parameters of Ca2+ dynamics in brain preparations (45Ca-uptake to slices and [3H]nitrendipine binding to membrane fractions) were measured in naive and chronic morphine-administered rats. While morphine did not have any effect on 45Ca-uptake to striatal slices in normal Krebs-Ringer solution, it inhibited K+-stimulated 45Ca-uptake to slices. Furthermore, the effect of morphine was antagonized by naloxone. Inhibition of K+-stimulated 45Ca-uptake to striatal slices by morphine was not observed in preparations obtained from chronic morphine-administered rats (6 mg/kg/b.i.d./7 days). In membrane fractions, [3H]nitrendipine binding increased by 34% in striatum following chronic morphine treatment, whereas no change was observed in the cortex and hippocampus. The results will be discussed in relation to the phenomena underlying chronic morphine administration. 相似文献
Phosphatidylinositol 4-kinase IIα (PtdIns4KIIα) localizes to the trans-Golgi network and endosomal compartments and has been implicated in the regulation of endosomal traffic, but the roles of both its enzymatic activity and the site of its action have not been elucidated. This study shows that PtdIns4KIIα is required for production of endosomal phosphatidylinositol 4-phosphate (PtdIns(4)P) on early endosomes and for the sorting of transferrin and epidermal growth factor receptor into recycling and degradative pathways. Depletion of PtdIns4KIIα with small interfering RNA significantly reduced the amount of vesicular PtdIns(4)P on early endosomes but not on Golgi membranes. Cells depleted of PtdIns4KIIα had an impaired ability to sort molecules destined for recycling from early endosomes. We further identify the Eps15 homology domain–containing protein 3 (EHD3) as a possible endosomal effector of PtdIns4KIIα. Tubular endosomes containing EHD3 were shortened and became more vesicular in PtdIns4KIIα-depleted cells. Endosomal PtdIns(4,5)P2 was also significantly reduced in PtdIns4KIIα-depleted cells. These results show that PtdIns4KIIα regulates receptor sorting at early endosomes through a PtdIns(4)P-dependent pathway and contributes substrate for the synthesis of endosomal PtdIns(4,5)P2. 相似文献
Rapid eye movement sleep behavior disorder (RBD) frequently occurs in synucleinopathies including multiple system atrophy, Parkinson’s disease, and dementia with Lewy bodies despite the clinical course of RBD being different between these disorders. Comparatively, the existence of RBD symptoms is relatively rare in patients with progressive supranuclear palsy, a tauopathy showing atypical parkinsonism compared with Parkinson’s disease. Moreover, in patients with Alzheimer’s disease, which is another tauopathy, RBD symptoms are less frequent than dementia with Lewy bodies, although both disorders share commonalities in terms of the existence of cortical dementia. Thus, RBD is thought to be relatively specific to synucleinopathies.
Plant leaf epidermal cells exhibit a jigsaw puzzle–like pattern that is generated by interdigitation of the cell wall during leaf development. The contribution of two ROP GTPases, ROP2 and ROP6, to the cytoskeletal dynamics that regulate epidermal cell wall interdigitation has already been examined; however, how interactions between these molecules result in pattern formation remains to be elucidated. Here, we propose a simple interface equation model that incorporates both the cell wall remodeling activity of ROP GTPases and the diffusible signaling molecules by which they are regulated. This model successfully reproduces pattern formation observed in vivo, and explains the counterintuitive experimental results of decreased cellulose production and increased thickness. Our model also reproduces the dynamics of three-way cell wall junctions. Therefore, this model provides a possible mechanism for cell wall interdigitation formation in vivo. 相似文献