scholarly journals Oxidative Cell Damage in Kat-sod Assay of Inorganic Halogen Compounds and Their Formation by Ozonation (Proceedings of the 23rd Symposium on Toxicology and Environmental Health)

Eisei kagaku ◽  
1998 ◽  
Vol 44 (1) ◽  
pp. P8-P8
Author(s):  
Hitoshi UENO ◽  
Koji OISHI ◽  
Yasuyoshi SAYATO ◽  
Katsuhiko NAKAMURO
Keyword(s):  
Environmental Health ◽  
Cell Damage ◽  
Halogen Compounds ◽  
Sod Assay

scholarly journals Interaction between Cadmium and Zinc on Cell Damage and Its Possible Mechanisms (Proceedings of the 21st Symposium on Toxicology and Environmental Health)

Eisei kagaku ◽  
1996 ◽  
Vol 42 (1) ◽  
pp. P20-P20
Author(s):  
ATSUSHI MISHIMA ◽  
CHIKA YAMAMOTO ◽  
YASUYUKI FUJIWARA ◽  
MICHIKO SAKAMOTO ◽  
TOSHIYUKI KAJI
Keyword(s):  
Environmental Health ◽  
Cell Damage

Electron Probe Analysis of Vertebrate Smooth Muscle: Distribution of Ca and Ci

1976 ◽  
Vol 34 ◽  
pp. 334-335 ◽  
Author(s):  
Avril V. Somlyo ◽  
H. Shuman ◽  
A.P. Somlyo
Keyword(s):  
Smooth Muscle ◽  
Electron Probe ◽  
Preliminary Report ◽  
Cell Damage ◽  
Electron Probe Analysis ◽  
Perinuclear Space ◽  
Probe Analysis ◽  
High K ◽  
Low K ◽  
Initial Results

This is a preliminary report of electron probe analysis of rabbit portal-anterior mesenteric vein (PAMV) smooth muscle cryosectioned without fixation or cryoprotection. The instrumentation and method of electron probe quantitation used (1) and our initial results with cardiac (2) and skeletal (3) muscle have been presented elsewhere.In preparations depolarized with high K (K2SO4) solution, significant calcium peaks were detected over the sarcoplasmic reticulum (Fig 1 and 2) and the continuous perinuclear space. In some of the fibers there were also significant (up to 200 mM/kg dry wt) calcium peaks over the mitochondria. However, in smooth muscle that was not depolarized, high mitochondrial Ca was found in fibers that also contained elevated Na and low K (Fig 3). Therefore, the possibility that these Ca-loaded mitochondria are indicative of cell damage remains to be ruled out.

Applications of CCEM to Environmental Health Problems

1985 ◽  
Vol 43 ◽  
pp. 102-103
Author(s):  
R. J. Lee ◽  
J. S. Walker
Keyword(s):  
Electron Microscopy ◽  
Image Analysis ◽  
Environmental Health ◽  
Computer Control ◽  
External Agent ◽  
External Agents ◽  
Computer Controlled ◽  
Primitive State ◽  
Textural Changes ◽  
General Aspects

Electron microscopy (EM), with the advent of computer control and image analysis techniques, is rapidly evolving from an interpretative science into a quantitative technique. Electron microscopy is potentially of value in two general aspects of environmental health: exposure and diagnosis.In diagnosis, electron microscopy is essentially an extension of optical microscopy. The goal is to characterize cellular changes induced by external agents. The external agent could be any foreign material, chemicals, or even stress. The use of electron microscopy as a diagnostic tool is well- developed, but computer-controlled electron microscopy (CCEM) has had only limited impact, mainly because it is fairly new and many institutions lack the resources to acquire the capability. In addition, major contributions to diagnosis will come from CCEM only when image analysis (IA) and processing algorithms are developed which allow the morphological and textural changes recognized by experienced medical practioners to be quantified. The application of IA techniques to compare cellular structure is still in a primitive state.

Histological evaluation of cochlear hair cell damage from noise-induced hearing loss in chinchillas

1990 ◽  
Vol 48 (3) ◽  
pp. 332-333
Author(s):  
R.V. Harrison ◽  
R.J. Mount ◽  
P. White ◽  
N. Fukushima
Keyword(s):  
Hair Cell ◽  
Evoked Potential ◽  
Cell Damage ◽  
Acoustic Trauma ◽  
Histological Evaluation ◽  
Cell Integrity ◽  
Functional Changes ◽  
Cochlear Hair Cell ◽  
Left And Right ◽  
Contralateral Ear

In studies which attempt to define the influence of various factors on recovery of hair cell integrity after acoustic trauma, an experimental and a control ear which initially have equal degrees of damage are required. With in a group of animals receiving an identical level of acoustic trauma there is more symmetry between the ears of each individual, in respect to function, than between animals. Figure 1 illustrates this, left and right cochlear evoked potential (CAP) audiograms are shown for two chinchillas receiving identical trauma. For this reason the contralateral ear is used as control.To compliment such functional evaluations we have devised a scoring system, based on the condition of hair cell stereocilia as revealed by scanning electron microscopy, which permits total stereociliar damage to be expressed numerically. This quantification permits correlation of the degree of structural pathology with functional changes. In this paper wereport experiments to verify the symmetry of stereociliar integrity between two ears, both for normal (non-exposed) animals and chinchillas in which each ear has received identical noise trauma.

Osmolarity and Artificial Cell Damage in Ischemic Myocardium

1990 ◽  
Vol 48 (3) ◽  
pp. 262-263
Author(s):  
Richard Montione ◽  
Muhammad Ashraf
Keyword(s):  
Cell Damage ◽  
Uranyl Acetate ◽  
Tissue Preservation ◽  
Rat Myocardium ◽  
En Bloc ◽  
Cellular Changes ◽  
Artificial Cell ◽  
Cacodylate Buffer ◽  
Isotonic Buffer ◽  
Perfusion Fixation

Osmolarity of a fixative vehicle has long been known to have an effect on the tissue preservation. An increase in tissue osmolarity occurs in ischemia-damaged tissue and affects the morphology. In this study, we examined cellular changes in ischemic rat myocardium induced by varying fixative toxicity.Rats were sacrificed by decapitation and the hearts immediately removed and retrogradily perfused through the aorta with anoxic Kurbs-Henseleit medium. Hearts were then placed in a bag with a small amount of medium at 37°C for 90 minutes. Hearts were perfusion-fixed using 2% glutaraldehyde in 0.1 M cacodylate buffer pH -7.3 at three osmolarities. The isotonic buffer was adjusted to 311 mOsm/kg using D-manitol. Hypertonic buffers were adjusted to 375 and 400 mOsm/kg. One-half hour after perfusion fixation, the hearts were sliced and cut into small blocks and allowed to fix overnight at 4°C. Blocks were post fixed in osmium, en bloc stained in uranyl acetate, dehydrated in ethanol and embedded in Spurr medium.

Glutamine synthelase in the mechanism of ammonia-induced gastric mucosal cell damage

2001 ◽  
Vol 120 (5) ◽  
pp. A149-A149
Author(s):  
Y KUBOTA ◽  
K KATO ◽  
S OHARA ◽  
T SHIMOSEGAWA
Keyword(s):  
Cell Damage ◽  
Mucosal Cell ◽  
Gastric Mucosal Cell

Alpha-Tocopherol Protects Cultured Human Cells from the Acute Lethal Cytotoxicity of Dioxin

2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Damage ◽  
Smooth Endoplasmic Reticulum ◽  
Dehydroascorbic Acid ◽  
Human Cells ◽  
Alpha Tocopherol ◽  
Cervical Cancer Cells ◽  
Cultured Human Cells ◽  
Nuclear Damage ◽  
Conjunctival Epithelial Cells

The possible protection of cultured human cells from acute dioxin injury by antioxidants was investigated. The most potent dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), caused vacuolization of the smooth endoplasmic reticulum and Golgi apparatus in cultured human conjunctival epithelial cells and cervical cancer cells. Subsequent nuclear damage included a deep irregular indentation resulting in cell death. A dosage of 30–40 ng/mL TCDD induced maximal intracellular production of H2O2 at 30 minutes and led to severe cell death (0–31% survival) at two hours. A dose of 1.7 mM alpha-tocopherol or 1 mM L-dehydroascorbic acid significantly protected human cells against acute TCDD injuries (78–97% survivals), but vitamin C did not provide this protection. These results indicate that accidental exposure to fatal doses of TCDD causes cytoplasmic free radical production within the smooth endoplasmic reticular systems, resulting in severe cytotoxicity, and that vitamin E and dehydroascorbic acid can protect against TCDD-induced cell damage.

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