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Obel, Niels ;Hansen, Birte ;Christensen, Margot M. ;Nielsen, Søren Lyhne ;Rungby, Jørgen
doi: 10.1177/096032719301200503pmid: 7902111
Cytotoxic effects of mercuric chloride, methyl mercury, and silver lactate on polymorphonuclear leucocytes have been examined by assaying superoxide anion formation capability and chemotaxis of metal-exposed cells. Both superoxide anion formation and chemotaxis were negatively affected by all three metal compounds. Both bacteriotoxic functions were affected in a dose-dependent fashion, the functional deficits were seen at doses not affecting cell viability. Dose-response curves were remarkably similar for all three compounds. The bacteriotoxic capacity of polymorphonuclear leucocytes may be hampered by mercury and silver.
Vanneste, Yves ;Lison, Dominique
doi: 10.1177/096032719301200504pmid: 7902112
1 This study was initiated to ascertain the possibility of biochemically monitoring the rhabdomyonecrosis that occurs after organophosphate poisoning. The evolution of different parameters has been assessed in the rat 6, 16, 24 and 48 h following 0.67 x LD50 of soman. 2 Acetylcholinesterase (AChE) was inhibited to 60% of the control value in the diaphragm at 6 and 16 h and serum ChE levels inhibited to an average of 30% of the control value. At 24 h, total blood, brain and diaphragm AChE were inhibited by 40, 69 and 38%, respectively. 3 Rhabdomyonecrosis lesions occurred in the diaphragm after 24 h and were accompanied by a concurrent increase in urinary creatine excretion rate (300% of the control) and serum total creatine phosphokinase activity (280% of the control). Calcium-activated neutral protease and phosphorylase a activities were elevated in the muscle at the same time. 4 These biochemical markers will prove useful for investigating the possible relationships between the different neuromuscular syndromes occurring in the course of an OP poisoning and potential therapeutic or protective pharmacological measures.
Abdel-Gayoum, A.A. ;Ali, B.H. ;Ghawarsha, K. ;Bashir, A.A.
doi: 10.1177/096032719301200505pmid: 7902113
1 Administration of gentamicin to rats at doses of 20, 40 or 80 mg kg-1 d -1 for 6 days induced nephrotoxicity exhibited by elevated plasma creatinine concentration and a decrease in alkaline phosphatase activity in rat kidney cortex. 2 Gentamicin treatment produced significant elevation in plasma total cholesterol amounting to 70% at the 80 mg kg-1 dose. At this dose, the combined cholesterol fractions of low density and very low density lipoproteins increased by more than two-fold. 3 Gentamicin treatment also caused significant increase in plasma triglyceride concentration, while plasma phospholipid levels showed dose-dependent reductions. 4 In another experiment recovery of the aforementioned parameters was assessed 7 and 14 days after the withdrawal of gentamicin, administered at a dose of 40 mg kg-1 d-1 for 6 days. After 7 days from drug discontinuation, both plasma creatinine and total cholesterol concentrations returned to the control levels, while triglyceride concentration was still significantly higher than control 14 days after stoppage of treatment. 5 Plasma phospholipid concentration and the activity of cortical alkaline phosphatase were still significantly lower than control 14 days after cessation of the treatment.
Gao, M. ;Levy, L.S. ;Braithwaite, R.A. ;Brown, S.S.
doi: 10.1177/096032719301200506pmid: 7902114
1 Intratracheal instillation of sodium dichromate (CrVI) and chromium acetate hydroxide (CrIII) to male Wistar rats gave rise to increased chromium concentrations in whole blood, plasma and urine up to 72 h post exposure; peak concentrations were reached at 6 h after exposure. 2 The ratio of whole blood chromium to plasma chromium concentrations was significantly different for Cr(VI) and CR(III) treatments. Both blood chromium and plasma chromium assays should therefore be used for the assessment of chromium exposure. 3 Chromium was also detected in peripheral lymphocytes. Cr(VI), but not Cr(lll) accumulated significantly in the lymphocytes after treatment. These cells have potential to be used for biomarkers of the assessment of exposure to chromium compounds.
Lock, Edward A. ;Cross, Theresa J. ;Schnellmann, Rick G.
doi: 10.1177/096032719301200507pmid: 7902115
4-Aminophenol (PAP) is known to cause nephrotoxicity in the rat where it produces selective necrosis to renal proximal tubules. The aim of this work was to investigate the toxicity of PAP and its known nephrotoxic metabolite 4-amino-3-S-glutathionylphenol using a well defined suspension of rabbit renal proximal tubules. PAP at a concentration of 0.5 mM and 1 mM caused proximal tubule cell death (measured by lactate dehydrogenase release) in a time-dependent manner over a 4-h exposure. In contrast, 4-amino-3-S-glutathionylphenol at 1 mM produced no proximal tubule cell death over a similar 4-h exposure. At 2 h, 1 mM PAP inhibited proximal tubule respiration by 30% and decreased cellular adenosine triphosphate (ATP) levels by 60%. These events preceded cell death. The addition of PAP to proximal tubules led to a rapid depletion of cellular glutathione, exposure to 0.5 mM causing a 50% depletion within 1 h. The cytochrome P-450 inhibitors SKF525A (1 mM) and metyrapone (1 mM), the iron chelator deferoxamine (1 mM) and the antioxidant N,N'-phenyl-1,4-phenyienediamine (2 μM) had no effect on PAP-induced cell death. However ascorbic acid (0.1 mM), afforded a marked protection against the depletion of cellular glutathione and completely protected against the cell death produced by 1 mM-PAP. These results indicate that oxidation of PAP to generate a metabolite that can react with glutathione is an important step in the toxicity, while mitochondria appear to be a critical target for the reactive intermediate formed.
Meulenbelt, J. ;Dormans, J.A.M.A. ;van Bree, L. ;Rombout, P.J.A. ;Sangster, B.
doi: 10.1177/096032719301200508pmid: 7902116
1 In previous studies a rat inhalation model was developed to investigate the efficacy of treatment in acute NO2 intoxication. 2 Desferrioxamine was administered intravenously to study its effect on histological alterations in lung tissue in rats after acute NO2 exposure. 3 Twenty four hours after exposure to 175 ppm NO2 for 10 minutes the lung injury observed by light microscopy in the desferrioxamine treated rats was less pronounced than in the saline treated rats. 4 Desferrioxamine appeared to provide more protection with a dose of 100 mg kg-1 24 h-1 than with 200 mg kg-1 24 h-1.
Lewis, L.D. ;Essex, E. ;Volans, G.N. ;Cochrane, G.M.
doi: 10.1177/096032719301200509pmid: 8240851
1 The recent increase in asthma mortality coupledwith reports of fatal asthma associated with beta- 2-agonist therapy, has stimulated interest in the plasma concentrations of beta-2-agonists that produce systemic toxicity. 2 We prospectively studied 17 patients (9 male),mean age 23 years (range 2-72), who attendedthe emergency departments of hospitalsthroughout the United Kingdom having recently ingested an overdose of salbutamol. 3 Clinical, laboratory, ECG data, plasma and urine samples were obtained from each patient. Plasmawas assayed for salbutamol concentration using ahigh performance TLC-photodensitometric method. 4 The mean (± s.d.) salbutamol dose reported to have been ingested was 89(+83)mg and the mean plasma salbutamol concentration was 166 (range 18-449) ng ml potassium was 2.9 (s.d.±0.6) mM (n=16). None of-1. The mean plasma the patients in this study developed serious cardiac dysrrhythmias. 5 There were significant correlations between the plasma salbutamol concentration and plasma potassium concentration (r=-0.85; P<0.00005) and between plasma salbutamol concentration and pulse rate (r=0,66; P<0.005). 6 We conclude that in these patients, without respiratory decompensation, suprapharmacological plasma concentrations ofsalbutamol were tolerated without serious cardiac arrhythmias or any fatalities.
doi: 10.1177/096032719301200510pmid: 7902117
The effects of saline cathartics on the gastrointestinal transit time of activated charcoal were investigated in six healthy volunteers. The study shows that the mean gastrointestinal transit times of charcoal alone were 29.3 h and 24.4, 15.4, 17.3 and 17.5 h with sodium chloride, sodium sulphate, magnesium sulphate alone and Andrew's Liver Salt respectively. Some volunteers complained of slight abdominal discomfort in all the phases except the Andrew's Liver Salt phase.
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