This study was designed to investigate the effects of silkworm(Bombyx moril L.) powder on oxidative stress and membrane fluidity in brain membranes of rats. Sprague-Dawley(SD) male rats(160$\pm$10 g) were fed basic diet(control group), and experimental diets(SWP-200 and SWP-400 groups) added 200 and 400mg/kg BW/day for 6 weeks. There were no significant differences in cholesterol levels of brain memberanes by administration of silkworm powder (SWP). Membrane fluidities were significantly increased(21.5% and 30.8%, respectively) in brain mitochondria of SWP-200 and SWP-400 groups compared with control group, but significant difference between brain microsomes could not obtained. Basal oxygen radicals (BORs) in brain mitochondria and mircrosomes were significantly inhibited(8.5% and 16.5%, 16.8%and 24.8%, respectively) by SWP-200 and SEP-400 groups compared with control group. Induced oxygen radicals(IORs) in brain mitochondria were significantly inhibited(16.6% and 21.4%, respectively)by sWP-200 and SWP-400 groups compared with control group, but IOR in brain microsome were significantly inhibited about 16.0% by SWP-400 groups only compared with control group. Lipid peroxide(LPO) levels were significantly decreaed(14.8%and 22.4%, respectively) in brain mitochondria of SWP-200 and SWP-400 groups compared with control group, but LPO level was significantly decreased about 16.0% in brain microsome of SWP-400 group only. Oxidized protein(OP) levels were remarkably decreased(about 14.8% and 16.5%, respectively) in brain mitochondria of SWP-200 and SWP-400 groups, but OP level was significantly decreased about 13.0% in brain microsome of SWP-400 group only compared with control group, Theses results suggest that administration of in brain microsome of SWP-400 group only compared with control group. These results suggest that administration of SWP may play effective role in attenuating an oxidative stress and increasing a membrane fluidity in brain membranes.
This study was designed to investigate the effect of silkworm powder on oxygen radicals and their scavenger enzymes in brain membrances of SD rats. Hydroxyl radical (OH) levels resulted in a considerable decreases in brain mitochondria fraction. Superoxide radical (O$_2$) levels were a slightly decreased in brain cytosol fraction. Lipid peroxide (LPO) and Oxidized protein (OP) levels were significantly decreased in brain mitochondria and microsomes fraction. Mn-superoxide dismutase (SOD) activity was remarkably increased in the mitochondria fraction. Cu and Zn-SOD activities were effectively increased in brain cytosol fraction. GSHPx activity was considerably increased in brain cytosol fraction. These results suggest that anti-aging effect of silkworm plays an effective role in attenuating an oxidative stress and increasing a scravenger enzyme activity in brain membranes.
This study was designed to investigate the effects of silk fibroin powder (SFP : Mw 500) on oxidative stress and membrane fluidity in brain membranes of rats. Sprague-Dawley (SD) male rats (160$\pm$10 g) were fed basic diet (control group), and experimental diets (SFP-2.5 and SFP-5.0 groups) added 2.5 and 5.0 g/kg BW/day for 6 weeks. Cholesterol level was significantly decreased about 8.0% in brain microsomes of SFP-5.0 group only compared with control group. Membrane fluidities were significantly increased (12.9% and 15.2%, respectively) in brain microsomes of SFP-2.5 and SFP-5.0 groups, but significant difference between in brain mitochondria of these two groups could be not obtained. Basal oxygen radicals (BOR) in brain mitochondria and microsomes were significantly ingibited (10.4%, and 24.0%, 7.9% and 14.9%, respectively) by SFP-2.5 and SFP-5.0 groups compared with control group. Induced oxygen radicals (IOR) in brain mitochondria and microsomes were significantly inhibited (11.8% and 14.1%, respectively) by SFP-5.0 groups compared with control group compared with control group. Lipid peroxide (LPO) levels were dose-dependently decreased (12.9% and 21.9%, 13.2% and 22.5%, respectively) in brain mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group. Oxidized protein (OP) levels were significantly decreased (15.7% and 17.1%, 16.7% and 15.7%, respectively) in brain mitochondria and microsomes of SFP-2.5 and SFP-2.5 and SFP-5.0 groups compared with control group. These results suggest that administration of SFP may play an effective role in a attenuating a oxidative stress and increasing a membrane fluidity in brain membranes.
The effect of mulberry (Morus alba L.) leaf extract(MLE) on oxidative stress and membrane fluidity in brain membranes of SD rats fed with 100 and 300 mg/kg BW/day were carried out for 6 weeks. Cholesterol accumulations resulted in a consistent decreases (4.6% and 5.6%, respectively) in brain mitochondria and microsomes of MLE-300 group compared with control group. Membrane fluidities were dose-dependently increased (2.2% and 5.1%, 5.0% and 15.2%) in brain mitochondria and microsomes of MLE-100 and MLE-300 groups compared with control group. Basal oxygen radicals(BORs) in brain mitochondria and microsomes were significantly inhibited (15.7% and 25.1%, 9.0% and 12.4%, respectively) by MLE-100 and MLE-300 groups compared with control group. Induced oxygen radicals(IORs) in brain mitochondria and microsomes were significantly inhibited (8.9% and 13.1%, 16.5% and 23.2%, respectively) by MLE-100 and MLE-300 groups compared with control group. Lipid peroxide (LPO) levels were significantly decreased (8.5% and 18.1%, 7.6% and 12.3%) in brain mitochondria and microsomes of MLE-100 and MLE-300 groups compared with control group. Oxidized protein (OP) levels were dose-dependently decreased (4.3% and 14.2%, 10.0% and 10.9%, respectively) in brain microsomes of MLE-100 and MLE-300 groups compared with control group. These results suggest that MLE may play an effective role in an attenuating an oxidative stress and increasing a membrane fluidity in brain membranes.
This study was designed to investigate the effects of sea tangle (Laminaria japonica) extract and fucoidan components on anti-aging action. Sprague-Dawley(SD) male rats (210$\pm$5g) were fed experimental diets Dasi-Ex group: sea tangle extract powder of 4.0% added to control diet; Fuco-I, II and III groups: funcoidan powder of 1, 2 and 3% added to Dasi-Ex group for 45 days. Hydroxyl radical (.OH) formations were significantly inhibited (10-20% and 25-30%) in serum and brain mitochondria of Dasi-Ex and Fuco-I, II and III groups compared with control group. Significant differences in .OH formations of brain mitochondria in Dasi-Ex and Fuco-I groups could not be obtained, but.OH formations of brain microsomes resulted in a significant decrease (15-20%) in Fuco-II and III groups compared with control group. Basal oxygen radical (BOR) formations were significantly decreased about 10% and 13-15% in brain mitochondria of Dasi-Ex and Fuco-I group, and Fuco-II, III groups, and also decreased about 10% and 15-20% in brain microsomes of Dasi-Ex and Fuco-I groups, and Fuco-II, III groups. LPO levels of brain mitochondria and microsomes were significantly inhibited about 10% in Dasi-Ex and Fuco-I, II groups and 15% in Fuco-III groups. Oxidized proteins (>C=O) were significantly inhibited about 10% in serum of Dasi-Ex and Fuco-I, II, III groups and brain mitochondria of Dasi-Ex group, while remarkably inhibited (30~35%) in brain mitochondria of Fuco-I, II and III groups. Nitric oxide (NO) levels were significantly inhibited (12~15%) in serum of Fuco-I, II and III groups, but there no significant difference in serum NO levels of Dasi-Ex group. Superoxide dismutase (SOD) activities were remarkably increased (30~ 60%) in serum of Fuco-I, II and III groups, but there were no significant differences in SOD activities in serum of Dasi-Ex group. Catalase (CAT) activities were significantly increased about 20% in serum of Dasi-Ex and Fuco-I, II, III groups. Mn-SOD activities in brain mitochondria were significantly increased about 17% in Dasi-Ex group, while remarkably increased 26~36% in Fuco-I, II, III groups. Cu,Zn-SOD activities in brain cytosol were dose-dependently of fucoidan increased 10%, 12% and 18%, respectively, compared with control group. These results suggest that anti-aging effects of fucoidan may play a pivotal role in attenuating a various age-related changes such as chronic degenerative disease and senile dementia.
The present study elucidated the effect of $\beta$-carbolines (harmaline and harmalol) on brain mitochondlial dysfunction caused by the tyrosinase-induced oxidation of dopamine. Harmaline, harmalol and antioxidant enzymes (SOD and catalase) attenuated the dopamine-induced alteration of membrane potential, cytochrome c release and thiol oxidation in mitochondria. In contrast, antioxidant enzymes failed to reverse mitochondrial dysfunction induced by dopmnine plus tyrosinase. $\beta$-Carbolines decreased the damaging effect of dopamine plus tyrosinase against mitochondria, except no effect of harmalol on thiol oxidation. Antioxidant enzymes decreased the melanin formation from dopamine in the reaction mixture containing mitochondria but did not reduce the formation of dopamine quinone caused by tyrosinase. Both harmalol and harmaline inhibited the formation of reactive quinone and melanin. Harmalol being more effective for quinone formation and vise versa. The results indicate that compared to MAO-induced dopamine oxidation, the toxic effect of dopamine in the presence of tyrosinase against mitochondria may be accomplished by the dopamine quinone and toxic substances other than reactive oxygen species. $\beta$-Carbolines may decrease the dopamine plus tyrosinase-induced brain mitochondrial dysfunction by inhibition of the formation of reactive quinone and the change in membrane permeability.
This study was designed to investigate the effects of mulberry (Morus alba L.) leaf extract (MLE) on oxygen radicals and their scavenger enzymes in brain membranes of rats. Sprague-Dawley (SD) male rats (160$\pm$10 g) were fed basic diet (control group), and experimental diets (MLE-100 and MLE-300 groups) added 100 and 300 mg/kg BW/day for 6 weeks. Hydroxyl radical (.OH) lecels resulted in significant decreases (13.4% and 21.1%, 12.0% and 13.4%, respectively) in brain mitochondria and microsome of MLE-100 and MLE-300 groups compared with control group. Superoxide radical ($O_2$) levels were significantly decreased about 12% in brain cytosol of MLE-300 group compared with control group. Lipid peroxide (LPO) levels were effectively inhibited (18.1% and 12.3%, respectively) in brain mitochondria and microsomes of MLE-300 groups compared with control group. Oxidized protein (OP) levels were significantly decreased (14.2%, and 10.9%, respectively) in brain mitochondria and microsomes of MLE-300 groups compared with control group. Mn-SOD activities in brain mitochondria were significantly increased (13.5% and 18.6%, respectively) in MLE-100 and MLE-300 groups, and Cu/Zn-SOD activities in brain cytosol were also effectively increased (about 17.7%) in MLE-300 groups compared with control group. GSHPx activities in brain cytosol were remarkably increased (17.2% and 23.9%, respectively) in MLE-100 and MLE-300 groups compared with control group. These results suggest that anti-aging effect of mulberry leaf extract (MLE) may play a pivotal role in attenuating a various age-related changes in brain.
This study was designed to investigate the effects of silk fibroin(Mw 500) powder (SFP) on oxygen radicals and the scavenger enzymes in brain membranes of rats. Spragu-Dawley(SD) male rats(160${\pm}$10g) were fed basic diet(control group), and experimental diets(SFP-2.5 and SFP-5.0 groups) added 2.5 and 5.0g/kg BW/day for 6 weeks. Hydroxyl radical($.$OH) levels resulted in a decreases(6.6% and 9.7%, 2.8% and 11.9%, respectively) in brain mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group, but were significantly decreased in these membrances of SFP-5.0 group only. Superoxide radical (O2) levels were a slightly decreased (2.0% and 9.1%, respectively) in brain cytosol of SFP-2.5 and SFP-5.0 groups compared with control group. Lipid peroxide(LPO) levels were significantly decreased (12.9% and 21.9%, 13.2% and 22.5%, respectively) in brain mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group. Oxidized protein (OP) levels were significantly decreased (16.7% and 15.7%, respectively) in brain microsomes of SFP-2.5 and SFP-5.0 group compared with control group, but significantly difference between in brain mitochondria of these two groups could not be obtained. Mn-SOD activities were remarkably increased (11.2% and 24.2%, respectively) in mitochodria of SFP-2.5 and SFP-5.0 groups. CuZn-SOD activities were effectively increased (7.7% and 19.6%, respectively) in brain cytosol of SFP-2.5 and SFP-5.0 groups, but significant difference between control and SFP-2.5 groups could be not obtained. GSHPx activities were considerably increased (5.3% and 11.7%, respectively) in brain cytosol of SFP-2.0 and SFP-5.0 groups compared with control group. There results suggest that anti-aging effect of silk fibroin may play an effective learning and memory role in a attenuating a oxidative stress and increasing a scavenger enzyme activity in brain membranes.
The decrease of metabolism in the brain has been observed as the important lesions of Alzheimer's disease (AD) from the early stages of diagnosis. The cumulative evidence has reported that the failure of mitochondria, an organelle involved in diverse biological processes as well as energy production, maybe the cause or effect of the pathogenesis of AD. Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. In addition, mitochondria are involved in different biological processes depending on the specific functions of each cell type in the brain. Thus, it is necessary to understand mitochondrial dysfunction as part of the pathological phenotypes of AD according to each cell type. In this review, we summarize that 1) the effects of AD pathology inducing mitochondrial dysfunction and 2) the contribution of mitochondrial dysfunction in each cell type to AD pathogenesis.
The toxic effects of methylmercury on the ultrastructures of the brain and gill tissues of fightingfish and compensative effects of red ginseng were investigated by means of electron microscopy. The brain neuron of methylmercury exposure group showed dilatation of dendrite and axon, numerical decrease of ribosomes, partial loss of nucleoplasm and cytoplasm and considerable swelling of mitochondria as compared with the normal neuron. And necrotic cell with ruptured nucleus and vacuolated mitochondria was noticeable. While, slight swelling of mitochondria, some dilation of dendrite and axon and numerical increase of ribosome occurred in the neuron of methylmercury-red ginseng treatment group as compared with the methylmercury exposure group. In the gill lamella of methylmercury exposure group, collapse of pillar cells and arms, dilated epithelial cell and thickened membrane were observed. While, in the gill lamella of methylmercury-red ginseng treatment group, arms were slightly disintegrated and basement membrane was some thickend as compared with the methylmercury exposure group. From the above results, it is concluded that red ginseng has detoxication effect on methylmercury toxicity and so takes compensative effect on injured tissues caused by methylmercury intoxication.
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