scholarly journals Strong Acute Toxicity, Severe Hepatic Damage, Renal Injury and Abnormal Serum Electrolytes after Intravenous Administration of Cadmium Fluoride in Rats

2007 ◽  
Vol 49 (3) ◽  
pp. 235-241 ◽  
Author(s):  
Kazuya Adachi ◽  
Tomotaro Dote ◽  
Emi Dote ◽  
Go Mitsui ◽  
Koichi Kono
Keyword(s):  
Acute Toxicity ◽  
Intravenous Administration ◽  
Renal Injury ◽  
Hepatic Damage ◽  
Serum Electrolytes ◽  
Cadmium Fluoride

scholarly journals Acute Lethal Toxicity, Hyperkalemia Associated with Renal Injury and Hepatic Damage after Intravenous Administration of Cadmium Nitrate in Rats

2007 ◽  
Vol 49 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Emi Dote ◽  
Tomotaro Dote ◽  
Hiroyasu Shimizu ◽  
Yukari Shimbo ◽  
Michiko Fujihara ◽  
...  
Keyword(s):  
Intravenous Administration ◽  
Renal Injury ◽  
Hepatic Damage ◽  
Cadmium Nitrate ◽  
Lethal Toxicity

scholarly journals Assesment of 28 days repeated adminstration toxicity profile of dexamethasone palmitate injection

2015 ◽  
Vol 27 (1) ◽  
pp. 9-19 ◽  
Author(s):  
Ganesh N Sharma ◽  
Shaili Rasania ◽  
Paresh Dadhaniya ◽  
Chintan Patel ◽  
Kapil Vachhani
Keyword(s):  
Acute Toxicity ◽  
Intravenous Administration ◽  
Adverse Reactions ◽  
Reference Range ◽  
Range Limit ◽  
Experimental Animals ◽  
Dexamethasone Palmitate ◽  
Laboratory Reference ◽  
Dose Levels ◽  
Different Levels

Although, the dexamethasone have been used for the managements, against various ailments as single API or in combination with other drugs as acetate or palmitate salt. However, Dexamethasone as palmitate salt has not been investigated so far for sub acute toxicity on intravenous administration. Therefore, an attempt has been made to investigate sub-acute toxicity of dexamethasone palmitate injection. The drug was administered in experimental animals at different dose levels (0.07, 0.18 and 0.44 mg/kg, b.w.), for 28 days, and alteration in biochemical and haematological parameters was recorded along with histological examinations. The result data revealed that intravenous administration of dexamethasone palmitate does not causes any significant alteration in experimental animals examined at different levels. The observed changes were either well established adverse effects of Dexamethasone or were in laboratory reference range limit. The intravenous administered doses of drug were found safer, although somewhat adverse reactions may be observed at higher dose level (s). DOI: http://dx.doi.org/10.3126/jnpa.v27i1.12145 Journal of Nepal Pharmaceutical Association 2014 Vol.XXVII: 9-19

scholarly journals Silver nanoparticles induced oxidative and endoplasmic reticulum stresses in mouse tissues: implications for the development of acute toxicity after intravenous administration

2016 ◽  
Vol 5 (2) ◽  
pp. 602-608 ◽  
Author(s):  
Rui Chen ◽  
Lin Zhao ◽  
Ru Bai ◽  
Ying Liu ◽  
Liping Han ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Endoplasmic Reticulum ◽  
Acute Toxicity ◽  
Intravenous Administration ◽  
Toxic Damage ◽  
Target Organs ◽  
Mouse Tissues

AgNPs cause toxic damage by gradually imposing stress impacts on the target organs in mice.

Activated protein C reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation

Blood ◽  
2000 ◽  
Vol 95 (12) ◽  
pp. 3781-3787 ◽  
Author(s):  
Akio Mizutani ◽  
Kenji Okajima ◽  
Mitsuhiro Uchiba ◽  
Takayuki Noguchi
Keyword(s):  
Intravenous Administration ◽  
Renal Injury ◽  
Protein C ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Activated Protein C ◽  
Factor Xa ◽  
Renal Tissue ◽  
Tissue Blood Flow ◽  
Leukocyte Activation

We examined whether activated protein C (APC) reduces ischemia/reperfusion (I/R)–induced renal injury by inhibiting leukocyte activation. In a rat model, intravenous administration of APC markedly reduced I/R-induced renal dysfunction and histological changes, whereas intravenous administration of dansyl glutamylglycylarginyl chloromethyl ketone–treated factor Xa (DEGR-FXa; active-site–blocked factor Xa), heparin or diisopropyl fluorophosphate–treated APC (DIP-APC; inactive derivative of ARC) had no effect. Furthermore, APC significantly inhibited the I/R-induced decrease in renal tissue blood flow and the increase in the vascular permeability, whereas neither DEGR-FXa, heparin, nor DIP-APC produced such effects. Renal I/R-induced increases in plasma levels of fibrin degradation products were significantly inhibited by APC, DEGR-FXa, and heparin. These observations suggest that APC reduces I/R-induced renal injury independently of its anticoagulant effects but in a manner dependent on its serine protease activity. Renal levels of tumor necrosis factor- (TNF-), rat interleukin-8, and myeloperoxidase were significantly increased after renal I/R. These increases were significantly inhibited by APC but not by DEGR-FXa, heparin, or DIP-APC. Leukocytopenia produced effects similar to those of APC. These findings strongly suggest that APC protects against I/R-induced renal injury not by inhibiting coagulation abnormalities but by inhibiting activation of leukocytes that play an important role in I/R-induced renal injury. Inhibition of leukocyte activation by APC could be explained by the inhibitory activity of TNF-.

A comparison of the acute pathology induced by 3-phenylamino-1,2-propanediol (PAP) and its mono-oleoyl ester in rodents with the toxic oil syndrome in man

1995 ◽  
Vol 14 (2) ◽  
pp. 217-220 ◽  
Author(s):  
P. Carthew ◽  
R.E. Edwards ◽  
B.M. Dorman ◽  
R.D. Verschoyle
Keyword(s):  
Acute Toxicity ◽  
Toxic Effect ◽  
Blood Vessels ◽  
Intravenous Administration ◽  
Pulmonary Thromboembolism ◽  
Intraperitoneal Administration ◽  
Postmortem Examination ◽  
Cooking Oil ◽  
Toxic Oil Syndrome ◽  
Rats And Mice

Phenylamino-1,2 propanediol (PAP) and its mono-oleoyl ester have been identified in samples of the cooking oil thought to be responsible for the Toxic Oil Syndrome (TOS) which occurred in Spain in 1981. The acute toxicity of PAP and its mono-oleoyl ester have been examined in rats and mice, after daily administration for periods of up to 14 days to determine whether these compounds could produce any of the pathologies of TOS. Even at the highest dose, the 1-mono-oleoyl ester of 3-phenylamino-1,2 propanediol did not cause any toxicity in rats or mice when given intraperitoneally. 3-Phenylamino-1,2 propane diol, however, was toxic when administered to rats by this route. After 6-10 consecutive daily doses of PAP, at the highest dose administered (350 mg kg-1), all of the rats became unwell. Postmortem examination showed that the major pathology present was massive pulmonary throm boembolism. Further investigations of the toxicity of PAP after intravenous administration showed that it was not directly vasotoxic. The pulmonary thromboembolism seen with intraperitoneally administered PAP was due to the toxic effect of PAP on the mesenteric tissue and blood ves sels, causing thrombosis which subsequently embolised the blood vessels in the lung. Intra-gastric administration of PAP caused no toxicity in rats. Comparatively, the pathology seen after intraperitoneal administration of PAP was not thought to be representative of the pathology of the toxic oil syndrome in man.

Activated protein C reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation

Blood ◽  
2000 ◽  
Vol 95 (12) ◽  
pp. 3781-3787 ◽  
Author(s):  
Akio Mizutani ◽  
Kenji Okajima ◽  
Mitsuhiro Uchiba ◽  
Takayuki Noguchi
Keyword(s):  
Intravenous Administration ◽  
Renal Injury ◽  
Protein C ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Activated Protein C ◽  
Factor Xa ◽  
Renal Tissue ◽  
Tissue Blood Flow ◽  
Leukocyte Activation

Abstract We examined whether activated protein C (APC) reduces ischemia/reperfusion (I/R)–induced renal injury by inhibiting leukocyte activation. In a rat model, intravenous administration of APC markedly reduced I/R-induced renal dysfunction and histological changes, whereas intravenous administration of dansyl glutamylglycylarginyl chloromethyl ketone–treated factor Xa (DEGR-FXa; active-site–blocked factor Xa), heparin or diisopropyl fluorophosphate–treated APC (DIP-APC; inactive derivative of ARC) had no effect. Furthermore, APC significantly inhibited the I/R-induced decrease in renal tissue blood flow and the increase in the vascular permeability, whereas neither DEGR-FXa, heparin, nor DIP-APC produced such effects. Renal I/R-induced increases in plasma levels of fibrin degradation products were significantly inhibited by APC, DEGR-FXa, and heparin. These observations suggest that APC reduces I/R-induced renal injury independently of its anticoagulant effects but in a manner dependent on its serine protease activity. Renal levels of tumor necrosis factor- (TNF-), rat interleukin-8, and myeloperoxidase were significantly increased after renal I/R. These increases were significantly inhibited by APC but not by DEGR-FXa, heparin, or DIP-APC. Leukocytopenia produced effects similar to those of APC. These findings strongly suggest that APC protects against I/R-induced renal injury not by inhibiting coagulation abnormalities but by inhibiting activation of leukocytes that play an important role in I/R-induced renal injury. Inhibition of leukocyte activation by APC could be explained by the inhibitory activity of TNF-.

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