Ultrastructure of the rat epiphyseal growth plate following chronic ethanol ingestion

1981 ◽  
Vol 33 (1) ◽  
pp. 381-384 ◽  
Author(s):  
Michael D. Fallon ◽  
Daniel T. Baran ◽  
R. Bruce Craig ◽  
Steven L. Teitelbaum
Keyword(s):  
Growth Plate ◽  
Chronic Ethanol ◽  
Ethanol Ingestion ◽  
Epiphyseal Growth Plate

Effects of Hypophysectomy on the Occurrence and Calcifiability of Matrix Vesicles in the Epiphyseal Growth Plate of Immature Rats

1980 ◽  
Vol 38 ◽  
pp. 578-579
Author(s):  
S. I. Coleman ◽  
W. J. Dougherty
Keyword(s):  
Growth Plate ◽  
Matrix Vesicles ◽  
Epiphyseal Growth Plate ◽  
Hard Tissue ◽  
Hormonal Factors ◽  
Post Surgery ◽  
Mineral Deposition ◽  
Thin Sectioning ◽  
Integral Role ◽  
Cellular Secretion

In the cellular secretion theory of mineral deposition, extracellular matrix vesicles are believed to play an integral role in hard tissue mineralization (1). Membrane limited matrix vesicles arise from the plasma membrane of epiphyseal chondrocytes and tooth odontoblasts by a budding process (2, 3). Nutritional and hormonal factors have been postulated to play essential roles in mineral deposition and apparently have a direct effect on matrix vesicles of calcifying cartilage as concluded by Anderson and Sajdera (4). Immature (75-85 gm) Long-Evans hooded rats were hypophysectomized by the parapharyngeal approach and maintained fourteen (14) days post-surgery. At this time, the animals were anesthetized and perfusion fixed in cacodylate buffered 2.5% glutaraldehyde. The proximal tibias were quickly dissected out and split sagittally. One half was used for light microscopy (LM) and the other for electron microscopy (EM). The halves used for EM were cut into blocks approximately 1×3 mm. The tissue blocks were prepared for ultra-thin sectioning and transmission EM. The tissue was oriented so as to section through the epiphyseal growth plate from the zone of proliferating cartilage on down through the hypertrophic zone and into the initial trabecular bone. Sections were studied stained (double heavy metal) and unstained.

Chronic Alcoholism Decreases Polyunsaturated Fatty Acid Levels in Human Plasma, Erythrocytes, and Platelets – Influence of Chronic Liver Disease

1997 ◽  
Vol 78 (02) ◽  
pp. 808-812 ◽  
Author(s):  
María-Luisa Pita ◽  
José-María Rubio ◽  
María-Luisa Murillo ◽  
Olimpia Carreras ◽  
Mariá-José Delgado
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Alcoholism ◽  
Chronic Liver ◽  
Chronic Ethanol ◽  
Ethanol Ingestion ◽  
Control Group ◽  
Docosatetraenoic Acid ◽  
Long Chain

SummaryThe effect of chronic ethanol ingestion on fatty acid composition of plasma, erythrocyte and platelet phospholipids and on plasma 6-keto-PGF1α was studied. Two groups of alcoholic subjects, one of them with chronic liver disease, were studied and compared to a control group of healthy subjects. Linoleic acid was not affected by alcoholism but its larger metabolites arachidonic acid (20:4n6) and docosatetraenoic acid (22: 4n6) tended to be lower in erythrocytes and platelets of both groups of alcoholic patients; the decrease was more marked in the presence of chronic liver disease. Docosahexaenoic acid (22:6n3) was markedly decreased in plasma, erythrocytes and platelets obtained from alcoholic patients with chronic liver disease. Plasma levels of 6-keto-PGF1α, a metabolite of prostacyclin (PGI2), remained unchanged. We conclude that chronic ethanol ingestion induces important changes in long-chain polyunsaturated fatty acids, mainly in platelets, and that these changes are exacerbated when patients suffer from chronic liver disease.

scholarly journals Effect of chronic ethanol ingestion on fatty acid oxidation by hepatic mitochondria.

1975 ◽  
Vol 250 (13) ◽  
pp. 5122-5129
Author(s):  
A I Cederbaum ◽  
C S Lieber ◽  
D S Beattie ◽  
E Rubin
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Chronic Ethanol ◽  
Ethanol Ingestion ◽  
Acid Oxidation

Effect of Chronic Ethanol Ingestion on Biochemical Circadian Rhythms in Wistar Rats

Alcohol ◽  
1999 ◽  
Vol 18 (2-3) ◽  
pp. 147-152 ◽  
Author(s):  
V Rajakrishnan ◽  
P Subramanian ◽  
P Viswanathan ◽  
V.P Menon
Keyword(s):  
Circadian Rhythms ◽  
Wistar Rats ◽  
Chronic Ethanol ◽  
Ethanol Ingestion

scholarly journals Chronic Ethanol Ingestion Increases Superoxide Production and NADPH Oxidase Expression in the Lung

2006 ◽  
Vol 34 (3) ◽  
pp. 314-319 ◽  
Author(s):  
John A. Polikandriotis ◽  
Heidi L. Rupnow ◽  
Shawn C. Elms ◽  
Roza E. Clempus ◽  
Duncan J. Campbell ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Chronic Ethanol ◽  
Superoxide Production ◽  
Ethanol Ingestion

Effects of cyclophosphamide on the femural epiphyseal growth plate in young Sprague-Dawley rats

2002 ◽  
Vol 60 (4) ◽  
pp. 208-212 ◽  
Author(s):  
Oded Zilberman ◽  
Margareta Näsman ◽  
Carl-Magnus Forsberg ◽  
Sven Lindskog
Keyword(s):  
Growth Plate ◽  
Sprague Dawley ◽  
Epiphyseal Growth Plate ◽  
Sprague Dawley Rats

Rat mitochondrial ATP synthase ATP5G3: cloning and upregulation in pancreas after chronic ethanol feeding

2001 ◽  
Vol 6 (2) ◽  
pp. 91-98 ◽  
Author(s):  
HA-SHENG LI ◽  
JI-YING ZHANG ◽  
BRYAN S. THOMPSON ◽  
XIAO-YING DENG ◽  
MICHAEL E. FORD ◽  
...  
Keyword(s):  
Atp Synthase ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Metabolic Stress ◽  
Nuclear Gene ◽  
Chronic Ethanol ◽  
Ethanol Ingestion ◽  
Pancreatic Acinar Cells ◽  
Mitochondrial Atp Synthase ◽  
Ethanol Feeding

Individuals with chronic excessive alcohol ingestion are put at the risk of acute and chronic pancreatitis. Underlying molecular mechanisms are unknown. Differential gene expression in the pancreas was profiled using mRNA differential display by comparison between control and ethanol-consuming rats. Male Wistar rats were fed with diets containing 6.7% (vol/vol) ethanol for 4 wk. A cDNA tag that was overexpressed in the pancreas of rats fed ethanol was isolated. A 723-bp cDNA was cloned from a rat pancreatic cDNA library, which encodes a novel rat mitochondrial ATP synthase subunit 9, isoform 3 (ATP5G3), which is homologous to a human ATP5G3 gene. Real-time PCR demonstrated that all three nuclear gene isoforms (ATP5G1, ATP5G2, and ATP5G3) were consistently upregulated in the pancreas of alcohol-consuming rats, parallel with mitochondrial injury. The cellular response to mitochondrial damage and metabolic stress may reflect an adaptive process for mitochondrial repair in pancreatic acinar cells during chronic ethanol ingestion.

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