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Ultrastructural Damage (ultrastructural + damage)
Selected AbstractsMicrocystin extracts induce ultrastructural damage and biochemical disturbance in male rabbit testisENVIRONMENTAL TOXICOLOGY, Issue 1 2010Ying Liu Abstract In the present research, the changes of ultrastructures and biochemical index in rabbit testis were examined after i.p. injection with 12.5 ,g/kg microcystin (MC) extracts. Ultrastructural observation showed widened intercellular junction, distention of mitochondria, endoplasmic reticulum, and Golgi apparatus. All these changes appeared at 1, 3, and 12 h, but recovered finally. In biochemical analyses, the levels of lipid peroxidation (MDA) and H2O2 increased significantly at 1 h, indicating MC-caused oxidative stress. Finally, H2O2 decreased to the normal levels, while MDA remained at high levels. The antioxidative enzymes (CAT, SOD, GPx, GST) and antioxidants (GSH) also increased rapidly at 1 h, demonstrating a quick response of the defense systems to the oxidative stress. Finally, the activity of CAT, SOD, and GPX recovered to the normal level, while the activity of GST and the concentration of GSH remained at a high level. This suggests that the importance of MCs detoxification by GST via GSH, and the testis of rabbit contained abundant GSH. The final recovery of ultrastructure and some biochemical indexes indicates that the defense systems finally succeeded in protecting the testis against oxidative damage. In conclusion, these results indicate that the MCs are toxic to the male rabbit reproductive system and the mechanism underlying this toxicity might to be the oxidative stress caused by MCs. Although the negative effects of MCs can be overcome by the antioxidant system of testis in this study, the potential reproductive risks of MCs should not be neglected because of their wide occurrence. © 2009 Wiley Periodicals, Inc. Environ Toxicol 2010. [source] Hypoxia induces complex I inhibition and ultrastructural damage by increasing mitochondrial nitric oxide in developing CNSEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2008Sebastián Giusti Abstract NO-mediated toxicity contributes to neuronal damage after hypoxia; however, the molecular mechanisms involved are still a matter of controversy. Since mitochondria play a key role in signalling neuronal death, we aimed to determine the role of nitrative stress in hypoxia-induced mitochondrial damage. Therefore, we analysed the biochemical and ultrastructural impairment of these organelles in the optic lobe of chick embryos after in vivo hypoxia,reoxygenation. Also, we studied the NO-dependence of damage and examined modulation of mitochondrial nitric oxide synthase (mtNOS) after the hypoxic event. A transient but substantial increase in mtNOS content and activity was observed at 0,2 h posthypoxia, resulting in accumulation of nitrated mitochondrial proteins measured by immunoblotting. However, no variations in nNOS content were observed in the homogenates, suggesting an increased translocation to mitochondria and not a general de novo synthesis. In parallel with mtNOS kinetics, mitochondria exhibited prolonged inhibition of maximal complex I activity and ultrastructural phenotypes associated with swelling, namely, fading of cristae, intracristal dilations and membrane disruption. Administration of the selective nNOS inhibitor 7-nitroindazole 20 min before hypoxia prevented complex I inhibition and most ultrastructural damage. In conclusion, we show here for the first time that hypoxia induces NO-dependent complex I inhibition and ultrastructural damage by increasing mitochondrial NO in the developing brain. [source] Cryoprotective additives and cryostabilisation effects on muscle fillets of the freshwater teleost fish Rohu carp (Labeo rohita) during prolonged frozen storageJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 15 2006Shashi Kiran Jasra Abstract The effects of various cryoprotective additives separately and in combination were studied on the myofibrillar protein integrity, biochemical enzyme activity levels and muscle ultrastructure in the freshwater teleost fish Rohu carp (Labeo rohita). Fish muscle samples were divided into eight groups and immersed in different mixtures of cryoprotective additives (S1,S8), then frozen at , 20 or , 30 °C for 24 months. Electrophoretic studies revealed early (within 6 months) alteration of the myofibrillar proteins myosin light chain, ,-actinin and tropomyosin. Reduction of the storage temperature from , 20 to , 30 °C slowed down the degradative processes. Sodium dodecyl sulfate polyacrylamide gel electrophoresis indicated that fish muscle treated with cryoprotective mixture S8 (40 g L,1 sorbitol/3 g L,1 sodium tripolyphosphate/4 g L,1 sodium alginate) showed minimal post mortem changes in myofibrillar proteins. Ultrastructural results also revealed post mortem damage to the muscle, seen earliest (within 6 months) in the sample frozen-stored without additives (S2), as compared with the normal, unfrozen muscle (S1). The influence of cryoprotectants alone and in combination on fish muscle structural proteins, myosin and actin filaments (A and I bands), during prolonged frozen storage was investigated. After 12 months, samples frozen-stored with various cryoprotective additives (S2-S7), except S8, showed signs of myofibrillar disintegration. Beyond that time the degradative processes started showing up in all samples, with minimal muscle ultrastructural damage in sample S8. Again, reducing the storage temperature from , 20 to , 30 °C slowed down the degradative processes. Ultrastructural results correlated well with levels of biochemical enzymes (Ca2+ myofibrillar ATPase and succinic dehydrogenase) during frozen storage. This is the first report of the cryoprotective effects of these additives on this popular edible fish species. Of the various combinations of additives tested, cryoprotective mixture S8 was found to preserve the muscle structure longest under frozen storage conditions. However, even this mixture was only effective for 18 months at , 30 °C. Beyond that time the myofibrillar degradative processes were apparent with correlative electrophoretic, biochemical and ultrastructural studies. Copyright © 2006 Society of Chemical Industry [source] Manganese alters mitochodrial integrity in the hearts of swine marginally deficient in magnesium,BIOFACTORS, Issue 2 2004Kevin B. Miller Abstract It was previously reported that pigs marginally deficient in magnesium (Mg) and fed diets high in manganese (Mn) died suddenly with signs of sudden cardiac death. Manganese, which has properties similar to Mg, may exacerbate Mg-deficiency and be accumulated by mitochondria resulting in ultrastructural damage. The objective of this study was to determine whether deaths of the type previously observed were mediated by adverse interactions of Mn and Mg resulting in ultrastructural damage to the myocardium, alterations in electrocardiographic recordings and tissue retention of Mn, Mg and calcium (Ca). Forty-eight pigs were fed one of six diets in a 2 × 3 factorial arrangement of Mg (100 or 1000 mg Mg/kg) and Mn (5, 50 or 500 mg Mn/kg) for 8 weeks. Left ventricle muscle samples were collected for examination by transmission electron microscopy. No differences in heart muscle ultrastructure were observed between pigs fed low and adequate dietary Mg. However, marked myocardial necrosis and mitochondrial swelling were observed in pigs fed high dietary Mn when combined with low Mg. Feeding low dietary Mg elevated minimum (P < 0.01), maximum (P < 0.05) and average (P < 0.001) heart rates. Low dietary Mg resulted in a 55% probability of a ventricular beat being recorded (P = 0.05) and lower Mg (P < 0.02) and Ca (P < 0.04) contents in heart atria and ventricles. These results suggest that high Mn, when fed in combination with low Mg, disrupts mitochondrial ultrastructure and is associated with the sudden deaths previously reported. [source] | ||||||||||