scholarly journals Marrow Toxic Injury

2020 ◽  
Author(s):  
Keyword(s):  
Toxic Injury

Site of Lysosome Production During Hepatic Injury

1969 ◽  
Vol 27 ◽  
pp. 348-349
Author(s):  
Nalin J. Unakar
Keyword(s):  
Electron Microscopy ◽  
Golgi Apparatus ◽  
Mouse Liver ◽  
Hepatic Injury ◽  
Close Approximation ◽  
Experimental Conditions ◽  
Toxic Injury

The increased number of lysosomes as well as the close approximation of lysosomes to the Golgi apparatus in tissue under variety of experimental conditions is commonly observed. These observations suggest Golgi involvement in lysosomal production. The role of the Golgi apparatus in the production of lysosomes in mouse liver was studied by electron microscopy of liver following toxic injury by CCI4.

scholarly journals Enhanced Oxidative Stress and Physiological Damage inDaphnia magnaby Copper in the Presence of Nano-TiO2

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
W. H. Fan ◽  
M. M. Cui ◽  
Z. W. Shi ◽  
C. Tan ◽  
X. P. Yang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species Generation ◽  
Aquatic Organisms ◽  
Potential Hazard ◽  
Oxygen Species ◽  
Nano Tio2 ◽  
Physiological Regulation ◽  
Toxic Injury ◽  
Transfer Channel ◽  
Atpase Inhibition

This study examines the potential hazard of an individual nanomaterial on the Cu biotoxicity to aquatic organisms.Daphnia magnain the absence or presence of nano-TiO2was exposed to Cu. Maintaining nano-TiO2at a safe concentration cannot eliminate its potential hazard. The biomarkers superoxide dismutase, catalase, and Na+/K+-ATPase inD. magnawere measured. Cu in the presence of nano-TiO2induced higher levels of oxidative stress and physiological damage because of the sorption of Cu. Nano-TiO2also caused Na+/K+-ATPase inhibition possibly by impeding the Na+/K+transfer channel. The correlations among the biomarkers, mortality, and accumulation further showed that the overloading reactive oxygen species generation caused by nano-TiO2contributed to deeper oxidative stress and physiological regulation, thereby causing greater toxic injury.

In utero meconium passage in fetuses and newborns with myelomeningocele

2009 ◽  
Vol 3 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Enrico Danzer ◽  
Linda M. Ernst ◽  
Natalie E. Rintoul ◽  
Mark P. Johnson ◽  
N. Scott Adzick ◽  
...  
Keyword(s):  
Prussian Blue ◽  
Statistical Difference ◽  
Health Management ◽  
In Utero ◽  
National Institutes Of Health ◽  
Pathological Examination ◽  
Grading System ◽  
Fetal Life ◽  
Toxic Injury ◽  
Meconium Staining

Object The authors retrospectively investigated whether midgestational fetal myelomeningocele (fMMC) repair alters intrauterine meconium exposure. Methods Prior to the National Institutes of Health Management of Myelomeningocele Study, 54 fetuses underwent fMMC repair at the authors' institution. Forty-six fMMC sacs were available for pathological examination and 53 MMC sacs from postnatally repaired MMCs (pMMCs) were available for comparison. The presence and distribution of meconium were blindly evaluated using a grading system defined as follows: absent (no meconium present), mild (< 10 meconium-positive histiocytes [MPHs]/hpf), moderate (10–25 MPHs/hpf), and severe (> 25 MPHs/hpf). Hall's bile stain was used to confirm meconium and Prussian blue and Fontana Masson stains to exclude hemosiderin and melanin, respectively. Results Compared to pMMCs (79%), meconium histiocytosis was less prevalent in fMMC sacs (57%; p = 0.017). Meconium staining was completely absent in 43% of the fMMC sacs. Mild meconium histiocytosis was found in 35% fMMC and 61% pMMC sacs (p = 0.035). There was no statistical difference between groups with moderate and severe meconium histiocytosis. Conclusions Meconium passage in MMCs can occur early in fetal life. Fetal MMC repair may reduce the duration of meconium exposure, thereby potentially limiting the toxic injury to the vulnerable neural elements.

354 Growth arrest-specific protein 6 (GAS6) promotes liver tissue repair after an acute toxic injury

2006 ◽  
Vol 44 ◽  
pp. S135 ◽  
Author(s):  
F. Lafdil ◽  
V. Deveaux ◽  
M.N. Chobert ◽  
A. Brouillet ◽  
E.S. Zafrani ◽  
...  
Keyword(s):  
Liver Tissue ◽  
Tissue Repair ◽  
Growth Arrest ◽  
Specific Protein ◽  
Toxic Injury ◽  
Acute Toxic

scholarly journals Crotalus durissus sp. rattlesnake venom induces toxic injury in mouse sperm

Toxicon ◽  
2018 ◽  
Vol 153 ◽  
pp. 17-18 ◽  
Author(s):  
Fábio Henrique Fernandes ◽  
Eduardo Bustos-Obregon ◽  
Rosemary Matias ◽  
Doroty Mesquita Dourado
Keyword(s):  
Mouse Sperm ◽  
Toxic Injury ◽  
Rattlesnake Venom ◽  
Crotalus Durissus

scholarly journals Vernonia Amygdalina Del (Bitter Leaf) extract ameliorates isoniazid (INH) induced liver injury in Swiss Albino Mice

2018 ◽  
Author(s):  
Gebreselassie Addisu Tilaye ◽  
Muluken Fekadie Zerihun ◽  
Kasaw Adane Chuffa ◽  
Mahelet Arayaselassie ◽  
Daniel Seifu
Keyword(s):  
Liver Injury ◽  
Leaf Extract ◽  
Drug Clearance ◽  
Vernonia Amygdalina ◽  
Drug Induced ◽  
Standard Drug ◽  
Swiss Albino Mice ◽  
Antitubercular Drugs ◽  
Toxic Injury ◽  
Albino Mice

AbstractLiver plays a central role in the metabolism of drugs. Drug clearance and transformation exposes liver to toxic injury. Antitubercular drugs have been found to be hepatotoxic and potentially lead to drug-induced liver injury. Isoniazid is one of the most hepatotoxic first line antitubercular drugs. Conventional drugs used in the treatment of liver disease are often inadequate and a search for supplementation or alternative drugs for the treatment of hepatic damage is indispensible. Therefore our study aims to investigate the hepatoprotective potential of Vernonia Amygdalina Del (bitter leaf) extract against Isoniazid-induced liver injury in Swiss Albino Mice. Treatment of Mice orally with Vernonia Amygdalina Del extract at dose of 250mg/kg and 375 mg/kg significantly lowered (P<0.05) the serum level of liver enzymes in Isoniazid pretreated mice. The hepatoptotective activity of the extract found to be comparable with the standard drug, Silymarin (100 mg/kg, P.o.). Moreover, treatment with the extract significantly alleviated Isoniazid induced hepatic injury as supported by the photomicrographs of liver section of mice. The data shows aqueous Vernonia Amygdalina Del extract has a very promising hepatoprotective potential against isoniazid-induced liver injury.

scholarly journals Toxic Mechanisms of the Heart: A Review*

1990 ◽  
Vol 18 (4a) ◽  
pp. 583-596 ◽  
Author(s):  
Alan B. Combs ◽  
Daniel Acosta
Keyword(s):  
Chemotherapeutic Agents ◽  
Cardiovascular Pathology ◽  
Moderate Drinking ◽  
The Public ◽  
Toxic Injury ◽  
Convulsive Seizures ◽  
The Many ◽  
General Physical ◽  
New Evidence ◽  
Intrinsic Effect

Toxic injury is one of the many ways by which the functional integrity of the heart may become compromised. Any of the subcellular elements may be the target of toxic injury, including all of the various membranes and organelles. Understanding the mechanisms underlying cardiotoxicity may lead to treatment of the toxicity or to its prevention. Doxorubicin and its analogs are very important cancer chemotherapeutic agents that can cause cardiotoxicity. Other agents which are cardiotoxic and which have profound public health implications include the alkaloid emetine in ipecac syrup, cocaine, and ethyl alcohol. The most important cardiotoxic mechanisms proposed for doxorubicin include oxidative stress with its resultant damage to myocardial elements, changes in calcium homeostasis, decreased ability to produce ATP, and systemic release of cardiotoxic humoral mediators from tissue mast cells. Each of the first 3 mechanisms can lead to each of the other 2, and the causal relationships between all of these mechanisms are not clear. New evidence suggests that doxorubicinol, one of the metabolites of doxorubicin may be the moiety responsible for cardiotoxicity. Several other potential mechanisms also have been proposed for doxorubicin. Emetine in ipecac syrup is the first aid treatment of choice for many acute toxic oral ingestions and the alkaloid, itself, is used to treat amebiasis. Cardiotoxicity occurs following chronic exposure, such as occurs therapeutically in amebiasis and with ipecac abuse by bulemics. A number of mechanisms are proposed for emetine cardiotoxicity, but the current mechanistic literature is quite scarce. Cocaine abuse recently has caught the public interest, in particular because of the drug-related sudden deaths of certain athletes. Cocaine can cause hypertension, arrhythmias, and reduced coronary blood flow, each of which can contribute to its lethality. However, it may be possible that cocaine sudden death episodes are more related to hyperthermia and convulsive seizures, rather than to cardiovascular toxicity. Chronic alcohol use leads to dilated cardiomyopathy and failure as part of the general physical degeneration that occurs with alcoholism. Several mechanisms are proposed for the cardiomyopathy, but only 2 things seem clear. The cardiotoxicity is due to an intrinsic effect of alcohol, rather than to malnutrition or co-toxicity, and abstinence is the only effective treatment for the cardiomyopathy. Recent articles indicate that very moderate use of alcohol may be beneficial and protect against cardiovascular-related morbidity. One explanation for these findings seems to be that the non-drinking groups, against whom the moderate drinking comparisons were made, were enriched in former drinkers with significant alcohol-related cardiovascular pathology.

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