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 Particles generated from numerous anthropogenic and/or natural sources, such as crystalline α-Fe2O3 nanoparticles, have the potential to damage lung cells. In our study we investigated the effects of these nanoparticles (12.5 µg/ml) on lipid peroxidation and the antioxidative system in MRC-5 lung fibroblast cells following exposure for 24, 48 or 72 h. Exposure to α-Fe2O3 nanoparticles increased lipid peroxidation by 81 %, 189 % and 110 % after 24, 48 and 72 h, respectively. Conversely, the reduced glutathione concentration decreased by 23.2 % and 51.4 % after 48 and 72 h of treatment, respectively. In addition, an augmentation of the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase and glutathione reductase within the interval between 48-72 h was noticed. Taking into account that the reduced glutathione level decreased and the malondialdehyde level, a lipid peroxidation product, remained highly increased up to 72 h of exposure, it would appear that the MRC-5 antioxidant defense mechanisms did not efficiently counteract the oxidative stress induced by exposure to hematite nanoparticles.
The study was designed to determine metabolic and hormonal responses to acute modification of body carbohydrate stores by exercise and subsequent meals and to find out whether the responses depend on the training status of subjects. Nine sedentary students and 10 endurance athletes took part in four experimental sessions. During control session, after overnight fast oxygen uptake and CO2 production were measured and blood glucose, free fatty acids (FFA), insulin (I), leptin (L), growth hormone (GH), testosterone (T), catecholamines, ACTH and cortisol were determined. The remaining sessions were preceded by 1.5 h exercise at 70% HRmax in the evening followed by 12-16 hrs fast till morning when subjects ate either high-carbohydrate (H-CHO) or low-carbohydrate (L-CHO) meal or fasted. Respiratory gases and blood samples were collected before and 2 hours after meal. In glycogen depleted subjects respiratory quotient (RQ), I, norepinephrine (NE) and L decreased, whilst other variables were unaltered. Changes in I and NE were greater in athletes than in sedentary subjects. After H-CHO RQ, blood glucose, I and NE increased and FFA, GH and T decreased. The latter effect was greater in athletes than in untrained subjects. After L-CHO, RQ was at the fasting level and FFA increased only in sedentary group. In both groups I increased and GH and T decreased. Neither meal affected L concentration. In conclusion, hormonal and metabolic changes observed after depleting carbohydrate stores resemble those occurring during starvation. Composition of the ingested meal affects postprandial metabolism, which additionally depends on the subjects’ training status.
Cooking oil deteriorates with repeated thermal exposure, resulting in appearance change and formation of oxygen radicals. Consumption of the deteriorated oil causes oxidative stress related to lipid metabolism. This study evaluated the effects of palm (Elaeis guineensis Jacq.) oil on hepatic histology, redox status, and cytochrome P450 (CYP) profiles. Adult female mice were orally given purified water (control), fresh, or reused palm oil (4.5 g/kg/day) daily for 16, 24, and 36 weeks. The livers were then collected for histological examination and for the evaluation of the redox system and CYP expression profiles. Treatment with fresh oil for 36 weeks resulted in some pyknosis and karyorrhexis in hepatic tissues, while reused oil resulted in more injuries to the nuclei with hepatic fat accumulation from week 24 onwards. Depletion in reduced glutathione (GSH) stores, with a significant decrease in the GSH/GSSG ratio, was observed with the reused oil but not with the fresh oil. The expression profiles of drug-metabolizing CYPs were significantly modulated; Cyp2c29, Cyp3a11, and Cyp3a13 were suppressed by both fresh and reused oil, while only the reused oil elevated Cyp2e1. The expression of Cyp4a10 and Cyp4a14, the key enzymes in lipid metabolism, were expectedly up-regulated by both. These findings suggest reused oil has a deleterious effect on hepatic ultrastructure, induces an imbalance of redox state, and causes Cyp2e1 activation-associated oxidative stress. It is therefore recommended that fresh rather than reused palm oil be used for cooking, and large-scale or long-term consumption be avoided to reduce the risk of liver damage and drug-interactions.
The supply of substrates to the respiratory chain as well as of other metabolites (e.g. ATP) into inner compartments of mitochondria is crucial to preprotein import into these organelles. Transport of the compounds across the outer mitochondrial mem­brane is enabled by mitochondrial porin, also known as the voltage-dependent an- ion-selective channel (VDAC). Our previous studies led to the conclusion that the transport of metabolites through the outer membrane of the yeast Saccharomyces cerevisiae mitochondria missing VDAC (now termed YVD AC 1) is considerably re­stricted. Therefore we expected that depletion of YVDAC1 should also hamper pro­tein import into the mutant mitochondria. We report here that YVD AC 1-depleted mi­tochondria are able to import a fusion protein termed pSu9-DHFR in the amount com­parable to that of wild type mitochondria, although over a considerably longer time. The rate of import of the fusion protein into YVD AC 1-depleted mitochondria is dis-tinctly lower than into wild type mitochondria probably due to restricted ATP access to the intermembrane space and is additionally influenced by the way the supporting respiratory substrates are transported through the outer membrane. In the presence of ethanol, diffusing freely through lipid membranes, YVDAC1-depleted mitochon- dria are able to import the fusion protein at a higher rate than in the presence of external NADH which is, like ATP, transported through the outer membrane by facilitated diffusion. It has been shown that transport of external NADH across the outer membrane of YVDAC1-depleted mitochondria is supported by the protein import machin- ery, i.e. the TOM complex (Kmita & Budziñska, 2000, Biochim. Biophys. Acta 1509, 86.94.). Since theTOMcomplex might also contribute to the permeability of themem-brane to ATP, it seems possible that external NADH and ATP as well as the imported preprotein could compete with one another for the passage through the outer mem- brane in YVDAC1-depleted mitochondria.
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