bluuebunny/crossref_metadata_2025_split huggingface dataset:
Corticosterone does not cause Testicular Toxicopathology in the Rat: Relevance to Methylxanthines, ACTH and Stress
Authors: Harvey P.W. , Er J. , Fernandes C. , Rush K.C. , Major I.R. , Cockburn A. 
Published: December 2008

1 Methylxanthines, ACTH and stress are well known to produce testicular pathology (e.g. seminiferous tubule atrophy). Methylxanthines, ACTH and stress alter hormone secretion, particularly from the pituitary-adrenocortical system. Consequently, it has recently been suggested that there may be a causal relationship between changes in endogenous physiological adrenocortical secretions, particularly corticosterone, and testicular pathology.1 2 This study tested the hypothesis that corticosterone mediates the testicular effects of both methylxanthine treatment and stress. Corticosterone was administered daily by subcutaneous injection to groups of 10 male rats at dose levels of 2 or 20 mg kg-1 in propylene glycol (1 ml kg-1) for 1 month (the shortest duration of methylxanthine or ACTH exposure known to produce testicular pathology). The highest dose of corticosterone resulted in plasma concentrations that closely matched values resulting from stress (200-700 ng ml-1) compared with controls (<25 ng ml-1). 3 The highest dose of corticosterone caused reduced body weight gain, lower thymus, adrenal, seminal vesicle and prostate weights, but did not induce any testicular pathology. 4 That a high, but physiologically relevant, dose of corticosterone did not cause testicular pathology in this experiment excludes this steroid in the direct aetiology of methylxanthine, ACTH and stress-induced testicular pathology. Other steroids secreted from the adrenal, in combination with corticosterone, may be involved.
Double Fatal Inhalation of Dichloromethane
Authors: Manno M. , Rugge M. , Cocheo V. 
Published: December 2008

1 Two cases of lethal poisoning following acute inhalation of extremely high concentrations of dichloromethane (DCM) are reported. The concentrations of the solvent found in the blood of the two subjects collected at autopsy and analysed by gas chromatography/ mass spectrometry (572 and 601 mg 1-1) were compatible with those measured in the air a few hours after the discovery of the bodies (up to 168,000 ppm).2 Extensive brain and lung oedema and congestion, microhaemorrhagic changes of the stomach and congestion in other organs were observed on macroscopic and microscopic examination of both subjects. In addition, and in both cases, high but not lethal carboxyhaemoglobin (COHb) levels (30%) were found in the blood collected at autopsy.3 Narcosis and respiratory depression due to the effect of DCM on the central nervous system (CNS) appear to have played a critical role in the death of the two men. However, biotransformation of the solvent to toxic metabolites, including carbon monoxide (via oxidative dehalogenation by the cytochrome P450-dependent mixed function oxidase system) or formaldehyde, formic acid, inorganic chloride and carbon dioxide (via the glutathione-S-transferase pathway) may have also contributed significantly to fatal toxicity.
Protection against Cyanide Poisoning by the Co-administration of Sodium Nitrite and Hydroxylamine in Rats
Authors: Bhattacharya R. , Jeevaratnam K. , Raza S.K. , Das Gupta S. 
Published: December 2008

1 The protectiveness of combined treatment with sodium nitrite (SN) and hydroxylamine (HA) in cyanide intoxication was investigated in male rats. 2 Pretreatment with equimolar dose of SN or HA produced a significant protection against cyanide poisoning as shown by the protection index (LD50 of cyanide in protected rats/LD50 of cyanide in saline-treated rats). 3 The co-administration of SN and HA as a split dose produced an optimal and sustained methaemoglobinaemia. 4 Pretreatment with combined SN and HA administration at different time intervals offered sustained protection against cyanide and resultant cytochrome oxidase inhibition. 5 Adjunction of sodium thiosulphate (STS) in the SN + HA regimen further augmented the protection against cyanide poisoning. 6 The results suggest that pretreatment with SN + HA co-administration could significantly reduce the toxic manifestation of cyanide.
Camelford Water Poisoning Accident; Serial Neuropsychological Assessments and Further Observations on Bone Aluminium
Authors: McMillan T.M. , Freemont A.J. , Herxheimer A. , Denton J. , Taylor A.P. , Pazianas M. , Cummin A.R.C. , Eastwood J.B. 
Published: December 2008

The serial cognitive assessment of ten individuals made between 8 and 26 months after the water at Camelford in Cornwall was accidentally contaminated with aluminium sulphate, showed consistent evidence of impairment of information processing and memory. There was no obvious relationship between these impairments and measurements of anxiety and depression. Serial bone biopsies in two individuals showed that the aluminium which was present 6 and 7 months after the accident had disappeared by 19 months. In the eight individuals biopsied 12-17 months after the accident the bone showed no stainable aluminium. Thus, aluminium deposited in the bone of normal individuals can disappear within 18 months. After an accident such as that at Camelford important evidence of toxicity is likely to be missed if an investigation is delayed. The abnormal neuropsychological findings indicate cognitive impairment, but whether this was caused by an acute episode of brain damage, or other causes such as the psychological effects of stress resulting from the accident, is uncertain.
Identification of Epithelial Cells in Bronchoalveolar Lavage
Authors: Finotto Susetta , Rado Vanda , Dal Vecchio Aldo , Milani Gianfranco , Fabbri Leonardo M. , Maestrelli Piero 
Published: December 2008

1 Damage to the bronchial epithelium occurs after the inhalation of toxic substances and allergens, and through virus infections and it may lead to increased desquamation of epithelial cells in bronchoalveolar lavage (BAL). 2 In this study we compared two methods of staining the epithelial cells of BAL, the conventional cytochemical May Grunwald-Giemsa stain (MGG) and an immunocytochemical technique using a monoclonal antibody anti-human cytokeratin (CK) detected with APAAP immuno-alkaline phosphatase. BAL was obtained from 13 subjects and the epithelial cells were cytocentrifuged either immediately after collection (fraction A) or after washing (fraction B). 3 Higher percentages of epithelial cells were identified in fraction A with CK (20.0 ± 5.1 %) than in fraction A with MGG (11.2 ± 2.3%), which recognized only ciliated epithelial cells. In fact a proportion of CK-positive cells (34%) in fraction A were not ciliated. Underestimation of epithelial cells by MGG compared to CK was more pronounced in fraction B (8.0 ± 2.9% and 22.9 ± 3.0%, respectively) as there was a relative loss of ciliated CK+ cells after washings. 4 These results suggest that immunocytochemical staining with an anti-cytokeratin monoclonal antibody is more sensitive than using the MGG stain in detecting epithelial cells in BAL.
Poisoning due to Insect and Scorpion Stings/Bites
Authors: Nhachi Charles F.B. , Kasilo Ossy M.J. 
Published: December 2008

1 A retrospective study, 1980 to 1989 inclusive, of hospital admission cases due to insect and scorpion stings or bites was carried out in the six main central hospitals of Zimbabwe's four main cities. 2 A total of 92 cases were recorded and analysed. This constituted 1.5% of all hospital admissions for poisoning which were analysed during that time. 3 Of the 92 cases the highest number of victims were seen in the 2-to-5-year age group (29.3%), followed by the 6-to-10-year age group (23.9%). In other age groups the incidence of poisoning was distributed approximately evenly with the 41 to 50 and the over 60-year age groups having the least number of victims, (2.2%). 4 The main groups of insects associated with poisoning were bees, 44.6%; wasps, 8.7%; and spiders 8.7%. A further 32.6% of the insect stings were not specified. Scorpion stings accounted for 5.4% of incidences. 5 No fatalities occurred. 6 Treatment consisted mainly of the administration of promethazine, as an antihistamine in 35% of the cases, steroids (16.5% of the cases), perhaps for their anti-allergic effects, and paracetamol, a mild analgesic, (14.7% of the cases). Interestingly, 22.6% of the cases were given an antibiotic (14.1 % of which were penicillins). Adrenaline was administered in only 1.7% of the cases. 7 The majority of the recorded cases, 49.4%, were hospitalized for at least a day and the average duration of hospitalization was 6.4 days.
Short-Term Effect of Various Doses of Cyclosporin A on Plasma Lipoproteins and its Distribution in Blood: An Experimental Study
Authors: Andrade R.J. , Lucena M.I. , Gonzalez-Correa J.A. , Garcia-Arias C. , Gonzalez-Santos P. 
Published: December 2008

Hyperlipidaemia commonly develops in both transplant recipients and experimental animals receiving cyclosporin A (CsA). However, the threshold of CsA induced-changes on lipoproteins and the role of parenteral vehicle (cremophor) has not been defined. Male Wistar rats were classified into five groups of six animals each and received CsA in cremophor vehicle at doses of 5, 10 or 20 mg kg-1 d-1, s.c., vehicle alone or saline for 7 d. Blood was obtained 24 h after the last dose and plasma was analysed. Plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein subfractions (HDL-2, HDL-3) were isolated by sequential ultracentrifugation and their content of cholesterol, triglyceride and phospholipid was determined. Whole blood and trough plasma CsA levels were measured by monoclonal radioimmunoassay. Plasma lipids did not differ significantly among the five groups. At a dose of 20 mg kg-1 d-1 of CsA VLDL cholesterol rose significantly (P<0.05). Administration of either CsA or cremophor vehicle increased HDL-2 phospholipids (P<0.05) and decreased HDL-3 cholesterol. There was not a linear relationship between whole blood and plasma CsA levels and increasing CsA doses. Short-term treatment with low doses of CsA have little influence on lipid profile in the rat. Changes on lipoprotein composition can be attributed mainly to cremophor vehicle, conceivably due to its ethanol content.
The Effects on Rat Thyroid Function of an Hepatic Microsomal Enzyme Inducer
Authors: Johnson S. , McKillop D. , Miller J. , Smith I.K. 
Published: December 2008

1 Following daily administration to male albino rats for 2 weeks, β-naphthoflavone (25 and 60 mg kg-1, i.p.) and phenobarbitone (100 mg kg-1, p.o.) produced their characteristic patterns of induction of P450-related enzyme activities. β-naphthoflavone also induced p-nitrophenol glucuronidation by 160% over controls, while phenobarbitone produced only a 45% induction of this conjugation activity.2 β-Naphthoflavone produced significant reductions in plasma thyroxine (T4) concentrations on days 4 and 16 and also decreased tri-iodothyronine (T3) on day 4. Thyroid-stimulating hormone (TSH) was significantly increased on day 16 by the higher dose of β-naphthoflavone. Thyroid weight was significantly increased at both dose levels on day 16 and liver weight was significantly increased on both days 4 and 16. No histopathological changes were seen in the liver or pituitary, but 30% of the animals showed minimal to mild follicular epithelial hypertrophy of the thyroid gland.3 Phenobarbitone had no effect on T4concentrations, but significantly decreased T3on day 4. TSH increased by 60% on day 16, but was not statistically significant compared with controls. Thyroid weight was significantly increased on day 16 and liver weight was significantly increased on days 4 and 16. Mild to moderate thyroid follicular epithelial hypertrophy and moderate hepatocyte hypertrophy occurred in all animals. No histopathological changes were seen in the pituitary.4 The early changes in T4and/or T3were probably due to increased hepatic clearance by induction of thyroxine glucuronidation with both compounds. Thyroid hypertrophy would be expected to follow as a result of activation of the hypothalamic-pituitary-thyroid axis. Data for the two compounds suggest some variation in the precise mechanism of action, which has not yet been fully elucidated.
An investigation of Urinary Creatine Excretion as a Potential Marker for Testicular Damage
Authors: Nahas Kamil , le Net Jean-Loic , Provost Jean P. , Tomaszewski Konrad E. 
Published: December 2008

1 This study assessed urinary creatine excretion as a marker for testicular atrophy. 2 Male rats received a single i.p. dose of 2-methoxyethanol at 0, 250 or 750 mg kg-1 and were sacrificed 2 d later. Urinary creatine and creatinine excretion were measured on days 0, 1 and 2. 3 Decreased testicular weights and histopathological assessment revealed dose-related testicular damage. 4 On day 1, at both doses of 2-methoxyethanol, urinary creatine levels increased and creatinine levels decreased, resulting in a dose-related increase in the creatine/creatinine ratio. On day 2, the creatine/creatinine ratio was elevated relative to controls, but was less marked than on day 1. 5 The study confirmed that creatine excretion is a potential marker for acute testicular damage.
Chromosomal Aberrations Induced by Methyl Parathion in Human Peripheral Lymphocytes of Alcoholics and Smokers
Authors: Sunil Kumar K.B. , Ankathil Raveendran , Devi K.S. 
Published: December 2008

1 Two different concentrations (0.08 and 0.16 μg ml-1) of methyl parathion (MP), a broad-spectrum insecticide, were tested on peripheral lymphocytes of healthy non-smoking non-alcoholics (CN), chronic smokers (SM) and alcoholics with smoking habit (ALSM). 2 SM and ALSM revealed a significant increase in chromosome aberration frequencies in peripheral lymphocytes compared to the CN group. 3 MP did not induce chromosomal aberrations in vitro in the CN group at either of the concentrations tested. 4 In SM and ALSM , MP induced a significant increase in chromosomal aberrations in vitro in peripheral lymphocytes at a concentration of 0.16 μg ml-1. 5 The results indicate that the damage induced by MP in peripheral lymphocytes is potentiated by smoking and alcohol intake.
Biochemical Changes Associated with Muscle Fibre Necrosis after Experimental Organophosphate Poisoning
Authors: Vanneste Yves , Lison Dominique 
Published: December 2008

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.
Plasma Lipid Profile in Rats with Gentamicin-Induced Nephrotoxicity
Authors: Abdel-Gayoum A.A. , Ali B.H. , Ghawarsha K. , Bashir A.A. 
Published: December 2008

1 Administration of gentamicin to rats at doses of 20, 40 or 80 mg kg-1d-1for 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-1dose. 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-1d-1for 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.
The Teratogenic Metabolites of Vitamin A in Women Following Supplements and Liver
Authors: Buss N.E. , Tembe E.A. , Prendergast B.D. , Renwick A.G. , George C.F. 
Published: December 2008

1 Ten healthy female volunteers were given 5 doses of retinol as the palmitate; 50 and 150 mg retinol as an oral supplement, 50 and 150 mg as fried calf liver (50 and 150 g) and 3, 9 or 30 mg by intra-muscular injection. 2 Plasma concentrations of retinyl palmitate were higher after 50 mg retinol given as an oral supplement compared with 50 mg as liver; there was no significant difference between the 150 mg doses. Plasma concentrations of retinol showed only small increases. 3 The peak plasma concentrations (Cmax) of all- trans-retinoic acid, the principal teratogenic metabolite of retinol, and the area under the concentration-time curve (AUC) were up to 20-times higher after supplements compared to the same dose as liver. Plasma concentrations of all- trans-4-oxo-retinoic acid, 13- cis-retinoic acid and 13- cis-4-oxo-retinoic acid showed smaller differences between supplements and liver. 4 Intra-muscular administration of 30 mg retinol gave retinyl palmitate concentrations similar to those found after the oral doses but did not increase circulating concentrations of the acid metabolites. 5 Based on the formation of all- trans-retinoic acid, liver and supplements are not of equivalent teratogenic potential. Advice to pregnant women on the consumption of liver based on the reported teratogenicity of vitamin A supplements should be reconsidered.
An Immunological Study on Workers Occupationally Exposed to Cadmium
Authors: Karakaya A. , Yücesoy B. , Sardas O.S. 
Published: December 2008

1 To assess the quantitative relation between exposure to airborne cadmium and various markers of immune function, 37 male workers were examined and compared with unexposed controls. 2 Blood cadmium concentrations were signficantly , higher in the exposed workers than in the unexposed, as was urine cadmium. 3 No differences in the serum immunoglobulin (IgG, IgM and IgA) levels between two popularions were observed, There was also no significant correlation between blood cadmium concentrations and serum immunoglobulin levels of both exposed and control groups, It has been found also that while monocyte counts signficantly increased, lymphocyte, neutrophil and oesinophil counts remained unchanged.
Deaths from Pesticide Poisoning in England and Wales: 1945-1989
Authors: Casey P. , Vale J.A. 
Published: December 2008

1 Data on deaths from pesticide poisoning occurring in England and Wales between 1945 and 1989 (no data are available for 1954) have been collated; pesticides were responsible for only 1012 (1.1 %) of the 87,385 deaths from poisoning (excluding those due to carbon monoxide) occurring over this 44 year period. At least 73% of all pesticide fatalities were due to suicide and overall there was a predominance of males (male:female ratio 2.4:1). No deaths from pesticide poisoning in children under 10 years have been reported since 1974 although almost 50% of suspected pesticide poisoning incidents involve this age group. 2 Herbicides were responsible for 787 (78%) fatal poisonings, 110 (11%) were caused by insecticides, 69 (6.8%) by rodenticides, 30 (3.0%) by wood preservatives and 16 (1.6%) by other pesticides. 3 The herbicide, paraquat, was responsible for 570 of 1012 (56%) deaths and, although there has been a progressive decline in the annual number of deaths from paraquat poisoning since 1982, paraquat remains the most common cause of fatal pesticide poisoning in England and Wales. 4 Sodium chlorate caused 113 (11.2%) deaths, most of these fatalities occurring between 1965 and 1983; only one death has been recorded since 1984. The phenoxyacetate herbicides resulted in 50 deaths; 2,4-D was implicated most commonly, Sixty-eight deaths were due to organophosphorus insecticides; demeton-S-methyl, malathion and mevinphos were involved most frequently. Only eight deaths resulted from organochlorine insecticides and two of these also involved an organophosphorus insecticide. 5 Although pesticide poisoning is an uncommon cause of admission to hospital in England and Wales, the mortality remains high at least in adult cases due to the suicidal ingestion of paraquat.
Lindane Haematotoxicity Confirmed by In vitro Tests on Human and Rat Progenitors
Authors: Parent-Massin D. , Thouvenot D. , Rio B. , Riche C. 
Published: December 2008

Blood dyscrasias such as aplastic anaemia and leukopenia are described following the use of lindane for agricultural purposes or against ectoparasites in animal and human health. In order to determine the involvement of lindane in these effects, an in vitro model of haematotoxicity evaluation has been used. Culture of haematopoietic progenitors, Colony Forming Unit-Granulocyte and Macrophage (CFU-GM), have been performed in the presence of lindane with increasing concentrations. Results showed that lindane was cytotoxic for human progenitors. They were one thousand times more sensitive to the lindane than rat CFU-GM. This cytotoxicity was observed with lindane concentrations similar to those measured in human blood in cases of acute intoxication and in fat tissues of exposed populations.
Vitamin C in CC14 Hepatotoxicity-A Preliminary Report
Authors: Ademuyiwa O. , Adesanya O. , Ajuwon O.R. 
Published: December 2008

1 The hepatotoxic effect of CC14 was studied in the rat by using 3 well established liver function tests (plasma glucose, bilirubin and proteins) as indices of hepatic integrity.2 The protective effect of vitamin C against this hepatotoxicity was also investigated.3 CC 14 (8 ml kg-1body weight) caused a decrease in the levels of plasma conjugated bilirubin, glucose and protein.4 Vitamin C (2 g kg-1body weight) prevented liver damage induced by CC14. The possible mechanisms of protection are highlighted.
Calcium Channel Blockin Drug Overdose: an Australian Series
Authors: Howarth D.M. , Dawson A.H. , Smith A.J. , Buckley N. , Whyte I.M. 
Published: December 2008

1 A descriptive case study of calcium channel-blocking drug (CCB) overdoses in the Hunter Region of NSW was performed to analyse the in-hospital morbidity and mortality of CCB drug overdoses in an Australian population. 2 The patients were admitted to major hospitals within the Hunter Region and treated initially with gastrointestinal decontamination, including the use of oral activated charcoal. Further management was required in most cases and included intravenous calcium, atropine and inotropic support. 3 Of the 15 CCB overdoses, four patients died. Non-cardiogenic pulmonary oedema occurred in two other cases. Cardiac conduction defects occurred in 11 cases. 4 Atropine was found to be effective only after intravenous calcium had been administered. 5 Overdose with slow-release verapamil required prolonged treatment with intravenous calcium salts. 6 Overdose with verapamil or diltiazem in doses greater than 300 mg carries a significant risk of death and potentially life threatening arrhythmias occur with lower doses. 7 Recommended initial management includes early, effective gastrointestinal decontamination. High dose intravenous calcium salts should be given to reverse hypotension and bradycardia. Atropine and inotropic support are frequently required.