Apoptosis precedes necrosis of dystrophin-deficient muscle

1995 ◽  
Vol 108 (6) ◽  
pp. 2197-2204 ◽  
Author(s):  
J.G. Tidball ◽  
D.E. Albrecht ◽  
B.E. Lokensgard ◽  
M.J. Spencer
Keyword(s):  
Structural Changes ◽  
Muscle Fibers ◽  
Microscopic Analysis ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Mdx Mice ◽  
Current View ◽  
Electron Microscopic ◽  
Preferential Cleavage ◽  
Tissue Sections ◽  
Necrotic Change

The current view that death of dystrophin-deficient muscle fibers is a necrotic process relies primarily upon the histological appearance of the tissue after the degenerative process is well advanced. Here, we tested this view by examining the possibility that apoptosis is a component of dystrophin-deficient muscle cell death. Three assays for apoptosis were employed in analyzing prenecrotic, peak necrotic and regenerated hindlimb muscle of mdx mice: (1) terminal deoxynucleotidyl transferase (TdT) mediated end-labeling of DNA in nuclei in tissue sections; (2) assays for DNA ladders; and (3) electron microscopic assays for the presence of organelles undergoing structural changes characteristic of apoptosis. At all ages sampled, mdx muscle contained apoptotic nuclei, according to TdT-mediated dUTP labeling of tissue sections. Nuclei in regenerated mdx muscle fibers did not display apoptosis. dUTP-labeled nuclei in control C57 muscles were rare or absent at all ages sampled. DNA from 4-week-old mdx mice was found to be cleaved into fragments indicative of preferential cleavage at internucleosomal sites. Electron microscopic analysis showed that organelle structural changes indicating apoptosis appear before pathological changes diagnostic of necrosis. For example, condensed mitochondria, fragmented sarcoplasmic reticulum and nuclei with chromatin condensations resembling apoptosis appear in fibers that otherwise possess normal morphology. Together, the findings show that apoptosis precedes any detectable necrotic change in mdx muscle, and that apoptotic events continue into the stage of dystrophic pathology that is currently viewed as necrosis. Thus, apoptosis characterizes the onset of pathology in dystrophin-deficient muscle which is followed secondarily by necrotic processes.

scholarly journals N-Acetylcysteine Attenuates Monocrotophos-induced Toxicity by Mitigating Oxidative Stress and Structural Changes in Rat Liver

2021 ◽  
Author(s):  
Jagjeet Singh ◽  
Annu Phogat ◽  
Chandra Prakash ◽  
Vijay Kumar ◽  
Vinay Malik
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Rat Liver ◽  
Protein Oxidation ◽  
Liver Tissue ◽  
Structural Changes ◽  
Microscopic Analysis ◽  
Stress Generation ◽  
Electron Microscopic ◽  
Pre Treatment

Abstract The present study evaluated the effect of N-acetylcysteine (NAC) against sub chronic monocrotophos (MCP) exposure induced oxidative stress in rat liver. Albino wistar rats were divided into control, NAC treated, MCP and MCP treated groups. An oral dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) was administered for 28 days. We observed high oxidative stress generation on MCP exposure in liver tissue as evident by significant increase in lipid peroxidation, protein oxidation and decreased glutathione content followed by altered activities of superoxide dismutase, catalase and acetylcholinesterase. Sub chronic MCP exposure caused an array of cellular and structural alternations in lipids and proteins of liver tissue as depicted by the FTIR, histopathological and electron microscopic analysis. N-acetylcysteine attenuated the loss of glutathione and prevented lipid peroxidation and protein oxidation. Pre-treatment of NAC also restored histological and ultra space structural alternations. So NAC protects oxidative stress and tissue damage induced by sub chronic MCP exposure in rat liver; suggesting the therapeutic and antioxidant potential of NAC.

Biochemical and Structural Changes in Mitochondria and Other Cellular Components of Pea Cotyledons During Germination

1972 ◽  
Vol 50 (7) ◽  
pp. 725-737 ◽  
Author(s):  
T. Solomos ◽  
S. S. Malhotra ◽  
S. Prasad ◽  
S. K. Malhotra ◽  
Mary Spencer
Keyword(s):  
Electron Microscopy ◽  
Structural Changes ◽  
Gradient Centrifugation ◽  
Microscopic Analysis ◽  
Sucrose Density Gradient ◽  
Electron Microscopic ◽  
Sucrose Density Gradient Centrifugation ◽  
Cellular Components ◽  
Further Development

Integrated studies comprising biochemical and electron microscopic analysis suggested that the increase in respiratory activity of pea cotyledon mitochondria during germination results from further development of the original mitochondria present in dormant seeds. Electron microscopy of isolated mitochondria as well as mitochondria in situ has revealed that membranes are scarce in the mitochondria present in dormant seeds. Mitochondrial cristae become well developed during the initial stages of germination. Crude mitochondrial preparations from pea cotyledons were fractionated by sucrose density gradient centrifugation and analyzed through electron microscopy. These studies showed that, at all stages of germination, "peroxisome"-like structures were present in the fractions of higher sucrose densities than that containing mitochondria. Biochemical studies revealed that the activities of catalase (H2O2:H2O2 oxidoreductase, EC 1.11.1.6) and peroxidase (guaicol:H2O2 oxidoreductase, EC 1.11.1.7) were associated mainly with these fractions and their activities increased during germination.

scholarly journals HIGH-RESOLUTION ELECTRON MICROSCOPIC ANALYSIS OF THE AMYLOID FIBRIL

1967 ◽  
Vol 33 (3) ◽  
pp. 679-708 ◽  
Author(s):  
Tsuranobu Shirahama ◽  
Alan S. Cohen
Keyword(s):  
Electron Microscopy ◽  
High Resolution ◽  
Amyloid Fibrils ◽  
Amyloid Fibril ◽  
Microscopic Analysis ◽  
High Resolution Electron Microscopy ◽  
Ultrastructural Organization ◽  
Electron Microscopic ◽  
Tissue Sections ◽  
Resolution Electron

The ultrastructural organization of the fibrous component of amyloid has been analyzed by means of high resolution electron microscopy of negatively stained isolated amyloid fibrils and of positively stained amyloid fibrils in thin tissue sections. It was found that a number of subunits could be resolved according to their dimensions. The following structural organization is proposed. The amyloid fibril, the fibrous component of amyloid as seen in electron microscopy of thin tissue sections, consists of a number of filaments aggregated side-by-side. These amyloid filaments are approximately 75–80 A in diameter and consist of five (or less likely six) subunits (amyloid protofibrils) which are arranged parallel to each other, longitudinal or slightly oblique to the long axis of the filament. The filament has often seemed to disperse into several longitudinal rows. The amyloid protofibril is about 25–35 A wide and appears to consist of two or three subunit strands helically arranged with a 35–50-A repeat (or, less likely, is composed of globular subunits aggregated end-to-end). These amyloid subprotofibrillar strands measure approximately 10–15 A in diameter.

scholarly journals IPTASE SYNTHESIS AND LIGHT MEDIATION IN TRANSGENIC TOBACCO

HortScience ◽  
1994 ◽  
Vol 29 (7) ◽  
pp. 737e-737
Author(s):  
Sandra L. Barbour ◽  
Margaret J. McMahon ◽  
John J. Frett ◽  
Dennis R. Decoteau
Keyword(s):  
Plant Growth ◽  
Transgenic Tobacco ◽  
Structural Changes ◽  
Polyclonal Antibodies ◽  
Red Light ◽  
Microscopic Analysis ◽  
Cellular Level ◽  
Cytokinin Activity ◽  
Electron Microscopic ◽  
Cytokinin Biosynthesis

Similarities exist between the effects of phytochrome and cytokinins on plant growth and development (e.g., chloroplast development, amaranthin synthesis. seed germination, photomorphogenesis). It is unclear, however, if and how these two systems interact. As a beginning step to determine cytokinin-phytochrome interactions, we developed a strategy utilizing ipt -transgenic tobacco in phytochrome/light treatment investigations. The sour-cc of the ipt gene was Agrobacterium tumefaciens Ti plasmid 15955. This gene encodes for isopentenyl transferase which is an enzyme active in cytokinin biosynthesis. Ipt -transgenic tobacco cultures (grown on MS medium supplemented with kanamycin but no plant growth regulators) were treated with end-of-day red or far-red light for 15 minutes. After 30 days of treatment, the plant tissue was harvested and either homogenized for SDS-PAGE or fixed for transmission electron microscopic analysis. Results from immuno-gold labelling using polyclonal antibodies specific to iptase will he used to Indicate the influence of phytochrome on cytokinin activity. Also, structural changes at the ultra-cellular level will be determined.

Morphology of Abnormal Columns of Mesenchyme Cells in the Channel Catfish, Ictalurus Punctatus.

1976 ◽  
Vol 34 ◽  
pp. 182-183
Author(s):  
Vernon Henderson
Keyword(s):  
Ictalurus Punctatus ◽  
Channel Catfish ◽  
Structural Changes ◽  
Microscopic Analysis ◽  
Common Source ◽  
Brood Stock ◽  
Electron Microscopic ◽  
Fin Ray ◽  
Fin Rays ◽  
Adipose Fin

During recent years , I have utilized several thousand young channel catfish or fry for several different studies. A few years ago, I noticed an increase in the number of adipose fins which showed fin ray-like structures. Fin rays in adipose fin of fish are rare. Assuming that the said structures were fin rays, I proceeded to study them, histologically. Upon microscopic examination, it was discovered that there was a complete absence of fin ray elements. In an effort to understand the structural changes responsible for the appearance of the ray-like elements , an electron microscopic analysis was undertaken.Fish used in this study were secured from several different catfish farms located in the Grambling area; however, all seem to be linked to a common source from which brood stock had been purchased. The specimen used in this study ranged in length from 7.5 centimeters to 15.0 centimeters and were approximately four to six months in age.

scholarly journals Heat Acclimation Regulates the Autophagy-Lysosome Function to Protect Against Heat Stroke-Induced Brain Injury in Mice

2017 ◽  
Vol 41 (1) ◽  
pp. 101-114 ◽  
Author(s):  
Junfeng Yi ◽  
Genlin He ◽  
Ju Yang ◽  
Zhen Luo ◽  
Xuesen Yang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Heat Stroke ◽  
Microscopic Analysis ◽  
Heat Acclimation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Electron Microscopic ◽  
Fluoro Jade B

Background/Aims: The mechanisms underlying the protective role of heat acclimation (HA) in heat stroke (HS)-induced brain injury are still unclear. The autophagy-lysosome pathway is known to pay an important role in protecting stressed or diseased cells from death. Nevertheless, whether autophagy and lysosomes are involved in HA-mediated neuroprotection following HS exposure remains unclear. Methods: The protective effects of HA were assessed by rectal temperature, hematoxylin-eosin staining, transmission electron microscopic analysis, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining, and Fluoro Jade B staining, after mice were subjected to HS. The effects of HA on autophagy and lysosomes were assessed in the presence of the autophagy inhibitor 3-methyladenine (3MA). Autophagy and lysosome-associated proteins were analysed by Western blotting. Results: We found that HA protected against HS-induced death and brain injury. HS can robustly induce autophagy and impair lysosome function. HA pre-conditioning significantly modulated the autophagy level, and improved lysosome function in HS mice. Furthermore, 3MA completely abolished the neuroprotective effect of HA on HS. Conclusion: HS may induce brain injury through lysosomal dysfunction and impaired autophagic flux. HA protected against HS-induced brain injury via a mechanism involving the autophagy-lysosome pathway.

scholarly journals Urinary C-type natriuretic peptide excretion: a potential novel biomarker for renal fibrosis during aging

2011 ◽  
Vol 301 (5) ◽  
pp. F943-F952 ◽  
Author(s):  
S. Jeson Sangaralingham ◽  
Denise M. Heublein ◽  
Joseph P. Grande ◽  
Alessandro Cataliotti ◽  
Andrew D. Rule ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Renal Fibrosis ◽  
Structural Changes ◽  
Microscopic Analysis ◽  
The Elderly ◽  
Electron Microscopic ◽  
Functional Changes ◽  
Age Related ◽  
Increased Risk ◽  
Renal Aging

Renal aging is characterized by structural changes in the kidney including fibrosis, which contributes to the increased risk of kidney and cardiac failure in the elderly. Studies involving healthy kidney donors demonstrated subclinical age-related nephropathy on renal biopsy that was not detected by standard diagnostic tests. Thus there is a high-priority need for novel noninvasive biomarkers to detect the presence of preclinical age-associated renal structural and functional changes. C-type natriuretic peptide (CNP) possesses renoprotective properties and is present in the kidney; however, its modulation during aging remains undefined. We assessed circulating and urinary CNP in a Fischer rat model of experimental aging and also determined renal structural and functional adaptations to the aging process. Histological and electron microscopic analysis demonstrated significant renal fibrosis, glomerular basement membrane thickening, and mesangial matrix expansion with aging. While plasma CNP levels progressively declined with aging, urinary CNP excretion increased, along with the ratio of urinary to plasma CNP, which preceded significant elevations in proteinuria and blood pressure. Also, CNP immunoreactivity was increased in the distal and proximal tubules in both the aging rat and aging human kidneys. Our findings provide evidence that urinary CNP and its ratio to plasma CNP may represent a novel biomarker for early age-mediated renal structural alterations, particularly fibrosis. Thus urinary CNP could potentially aid in identifying subjects with preclinical structural changes before the onset of symptoms and disease, allowing for the initiation of strategies designed to prevent the progression of chronic kidney disease particularly in the aging population.

scholarly journals N-Acetylcysteine Reverses Monocrotophos Exposure-Induced Hepatic Oxidative Damage via Mitigating Apoptosis, Inflammation and Structural Changes in Rats

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 90
Author(s):  
Jagjeet Singh ◽  
Annu Phogat ◽  
Chandra Prakash ◽  
Sunil Kumar Chhikara ◽  
Sandeep Singh ◽  
...  
Keyword(s):  
Antioxidant Enzyme ◽  
Inflammatory Cytokines ◽  
Rat Liver ◽  
Enzyme Activities ◽  
Structural Changes ◽  
Microscopic Analysis ◽  
Natural Antioxidants ◽  
Antioxidant Enzyme Activities ◽  
Electron Microscopic ◽  
Pro Inflammatory Cytokines

Oxidative stress-mediated tissue damage is primarily involved in hepatic injuries and dysfunctioning. Natural antioxidants have been shown to exert hepatoprotective, anti-inflammatory and antiapoptotic properties. The present study evaluated the effect of N-acetylcysteine (NAC) against monocrotophos (MCP) exposure-induced toxicity in the rat liver. Albino Wistar rats were divided into four groups: (1) control, (2) NAC-treated, (3) MCP-exposure, (4) NAC and MCP-coexposure group. The dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) were administered orally for 28 days. Exposure to MCP caused a significant increase in lipid peroxidation, protein oxidation and decreased glutathione content along with the depletion of antioxidant enzyme activities. Further MCP exposure increased pro-inflammatory cytokines levels and upregulated Bax and Caspase-3 expressions. MCP exposure also caused an array of structural alternations in liver tissue, as depicted by the histological and electron microscopic analysis. Thepretreatment of NAC improved glutathione content, restored antioxidant enzyme activities, prevented oxidation of lipids and proteins, decreased pro-inflammatory cytokines levels and normalized apoptotic protein expression. Treatment of NAC also prevented histological and ultrastructural alternations. Thus, the study represents the therapeutic efficacy and antioxidant potential of NAC against MCP exposure in the rat liver.

Structural Changes Leading to Spore Formation in the Myxosporidian Parasite Ceratomyxa Shasta Nobel

1977 ◽  
Vol 35 ◽  
pp. 338-339
Author(s):  
T. Yamamoto ◽  
R.L. Silliphant
Keyword(s):  
Structural Changes ◽  
Microscopic Analysis ◽  
Intestinal Epithelial ◽  
American Continent ◽  
Electron Microscopic ◽  
Connective Tissue Layer ◽  
Thin Sections ◽  
North American Continent ◽  
The North ◽  
Structural Details

Ceratomyxa shasta is a myxosporidian effecting mortalities of various species of salmonidae along the western regions of the North American continent.1,2 It is generally accepted from studies of myxosporidian infected t i ssues that the trophozoi tes undergo hi stozoi c development into multi- nucleated complexes which eventually form 2 characteristic spores in the mother cell. Most of the studies of Ceratomyxa have been with the light microscope3 and because of the small size of the parasite much of the structural details were not evident.For the electron microscopic analysis of the sporont and the developing spore of C. shasta two sources of experimentally infected specimens were examined. These were thin sections of free floating developmental forms from the gall bladder and thin sections of intestinal caecae fixed at 2, 7, 14 and 21 days following infection. The trophozoites measuring 20 μm in diameter were observed to increase in number by 14 days, infecting the connective tissue layer between the intestinal epithelial mucosa and the muscularis layer.

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