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Peritoneal toxicity of water: a model of chronic peritonitis caused by osmotic dysequilibrium in rats.

The purpose of this work was to determine whether the osmotic dysequilibrium created by intraperitoneal (i.p.) injection of pure water has any permanent, damaging toxic sequelae. Rats were injected i.p. with pure water on five successive days. Necropsies were performed 1 week after the last injection. Necropsies revealed fibrosis of peritoneal surfaces of liver and spleen, similar to the effects of chemical irritants but milder. The severity of the lesions depended on the dose of water and the number of injections. A few minutes of contact with pure water was sufficient to ensure subsequent development of fibrosis. Soon after the initial injury, the inoculum became less hypotonic and then isotonic. Isotonic or moderately hypotonic electrolyte solutions did not produce peritoneal fibrosis but very hypotonic solutions were toxic. Injection of the synthetic compound 48/80, which is known to cause discharge of mast cell granules, did not produce peritonitis, nor was contamination by endotoxin or by blood responsible for the lesions. Injection of water may be a useful method for investigating the role, if any, of mast cells and/or mesothelial cells in the toxic effects of osmotic dysequilibrium.

Animals↗

Redox metal chelation ameliorates radiation-induced bone marrow toxicity in a mouse model.

Since zinc desferrioxamine (Zn-DFO) has been shown to be a very potent protector against injuries induced by redox-active metal ions, we examined its protective effect against radiation-induced toxicity. We found that treatment with Zn-DFO given before TBI increased the survival of mice irradiated with 7.5 and 8.5 Gy. Zn-DFO also protected against radiation-induced myelosuppression and body weight loss, while soluble Il6 levels in serum were normalized in mice pretreated with Zn-DFO. We concluded that administration of Zn-DFO prior to TBI protected BALB/c mice from radiation-induced toxicity, increasing survival rates by up to 75%. The biological effect of Zn-DFO is known to result from its effect on the production of intracellular hydroxyl free radicals mediated by redox-active metal ions, and both metal chelation and zinc delivery appear to be equally likely mechanisms for this outcome. We suggest that radiation-induced toxicity is caused by the deleterious effect of redox-active metal ions, and that compounds which modulate this redox activity may act as radioprotectors.

Animals↗

Models for the effect of toxicant in single-species and predator-prey systems.

Models of single-species and predator-prey systems in a polluted closed environment are developed and partially analyzed. Three cases are considered: a single influx of toxicant, a constant influx of toxicant, and a periodic pollution of the environment. In the case of single-species growth we are able to determine some local and global dynamics. In the case of predator-prey systems, we investigate the existence of steady states for a small constant influx of toxicant.

Environmental Pollution↗

Physostigmine does not effect arousal but produces toxicity in an animal model of severe gamma-hydroxybutyrate intoxication.

OBJECTIVES: Physostigmine is an acetylcholinesterase inhibitor and can produce fasciculations, seizures, bradycardia, and asystole. gamma-hydroxybutyrate (GHB) increases acetylcholine levels in the central nervous system and can decrease heart rate. Despite this, physostigmine has been proposed as an arousal agent to treat coma from overdoses of GHB. The authors hypothesized that in the setting of severe GHB intoxication, physostigmine would reverse sedation without producing adverse effects such as a decrease in heart rate, seizures, and fasciculations. METHODS: GHB intoxication was induced in 20 rats by intraperitoneal injection of 700 mg/kg of the GHB precursor gamma-butyrolactone. One hour later, rats were randomly assigned to receive either physostigmine (0.06 mg/kg) intraperitoneally or an equivalent volume of saline. After administration of physostigmine, rats were continuously monitored by a blinded observer for arousal (return of righting reflex), fasciculations, and seizures. Heart rate and respiratory rate were recorded at 0, 5, 15, and 60 minutes after administration of physostigmine. Data were analyzed using repeated-measures analysis of variance and chi-square test. A pretest sample size calculation determined that 10 rats per group would detect a change in arousal from 0% to 50% and a 10% change in heart rate. RESULTS: No rats in either group had arousal within one hour (p = 1.0); however, ten of ten physostigmine-treated rats developed signs of physostigmine toxicity (fasciculations, 7; seizures, 3), while no controls developed signs of physostigmine toxicity (p = 0.00). The authors were unable to detect a decrease in heart rate. CONCLUSIONS: Physostigmine did not produce a 50% change in arousal as measured by a return of righting reflex but did produce physostigmine toxicity (fasciculations and seizures) in this rat model of severe GHB intoxication.

Animals↗

Use of iodine-123 metaiodobenzylguanidine scintigraphy for the detection of amiodarone induced pulmonary toxicity in a rabbit model: a comparative study with technetium-99m diethyltriaminepenta acetic acid radioaerosol scintigraphy.

The purpose of the study was; (i) to determine whether 123I-MIBG scintigraphy is sensitive for detection of amiodarone induced pulmonary toxicity (AIPT) and (ii) to compare it with 99mTc-DTPA radioaerosol. Twelve white New Zealand rabbit with initial mean body weight 4.24 +/- 0.47 g were divided into two groups. AIPT group (n = 7) was administered amiodarone (20 mg/kg BW). The control group (n = 5) received the same amount of 0.9% saline. All animals underwent 123I-MIBG and 99mTc-DTPA radioaerosol scintigraphy at the end of the treatment period. 123I-MIBG static thorax images were obtained during 10 minutes at 15 minutes and 3-hours after intravenous injection of the radiopharmaceutical. Lung to heart ratios (LHR) and lung to mediastinum ratios (LMR), and retention index (LRI) of 123I-MIBG were determined. Two days after 123I-MIBG scintigraphy, 99mTc-DTPA radioaerosol scintigraphy was performed, and clearance from the lungs was measured for 10 min (1 min/frame) following termination of inhalation. 123I-MIBG lung retention index (LRI) was significantly higher in the AIPT group than the control (61 +/- 4.6 vs. 40 +/- 4.5, p = 0.01). Early LHR and LMR were significantly lower in the AIPT group than in the control group (p = 0.04, p = 0.01, respectively), whereas those of late LHR and LMR were not significantly different. T1/2 values of DTPA clearance were significantly increased in AIPT group according to the control group (55 +/- 7.2 vs. 86.6 +/- 18.5, p = 0.02). 123I-MIBG scintigraphy is a valuable tool for detecting AIPT in a rabbit model. Additionally, 99mTc-DTPA radioaerosol scintigraphy is an excellent comprehensive investigational tool for detecting AIPT with the added advantage of lower cost.

3-Iodobenzylguanidine↗

Pulmonary vascular morphology in a fetal rabbit model for congenital diaphragmatic hernia.

BACKGROUND/PURPOSE: Although the pulmonary vascular abnormalities in congenital diaphragmatic hernia (CDH) are described from a morphologic point of view, the treatment of pulmonary hypertension (PH) remains one of the main unsolved problems in clinical daily practice. For this reason, detailed studies in well-validated animal models could still be of significance in our understanding of the pathogenesis of CDH. METHODS: In does of 23 days' gestational age (GA), 39 fetuses underwent creation of diaphragmatic hernia (DH) and 15 fetuses a sham thoracotomy (SHAM). Thirty-nine nonoperated littermates served as internal controls (CTR). Fetuses were harvested by cesarean section on days 25, 27, 29, and 30 of gestation. Lung specimens were obtained and formalin fixed for further vascular morphometry studies. RESULTS: Lung vessels from DH fetuses started to show significantly smaller internal diameter (ID), external diameter (ED), larger arterial wall thickness (WT), and, in particular, a proportionally higher medial thickness (%MT) and adventitial thickness (%AT) from day 27 onward when compared with control fetuses. SHAM fetuses, which were harvested at term, showed no differences with CTR. CONCLUSIONS: This is the first report documenting changes over time in the vascular system in a rabbit fetal model of surgically induced DH. These changes mimic pathologic findings observed in human fetuses and are also concordant with earlier observations in the surgical ovine model and the toxic nitrofen rat model.

Animals↗

Experimental model for heart failure in rats--induction and diagnosis.

BACKGROUND: Clinical heart failure is generally preceded by hypertrophy. Many animal models (e. g. toxic heart failure models) do not consider this hypertrophy. We set out to develop a heart failure model in rats by inducing pressure-overload hypertrophy. METHODS: We induced coarctation of the aortic arch with a tantalum clip (0.35 mm internal diameter) In 3-week-old rats (n=17). Starting at seven weeks postoperatively, we measured ejection fraction (EF), fractional shortening (FS), end-systolic (LVESD) and end-diastolic (LVEDD) left ventricular dimensions by echocardiography each week. Heart, lung, and liver specimens were analyzed histopathologically at least eleven weeks after the operation. RESULTS: Contractile function was significantly decreased in hearts from animals with aortic banding (EF: 45+/-5% vs. 73+/-5%, p<0.01; FS: 20+/-3% vs. 35+/-5%, p<0.01). At the same time, left ventricles were dilated (LVEDD: 9.1+/-0.6 mm vs. 7.4+/-0.5 mm; LVESD: 7.3+/-0.6 mm vs. 4.8+/-0.4 mm, p<0.01). These observations were associated with clinical and histopathological changes characteristic for chronic left heart failure. CONCLUSION: Placing a tantalum clip around the aortic arch in 3-week-old rats consistently induces left ventricular decrease in contractile function and dilatation after eleven weeks.

Animals↗

Toxicity assessment of industrial chemicals and airborne contaminants: transition from in vivo to in vitro test methods: a review.

Exposure to occupational and environmental contaminants is a major contributor to human health problems. Inhalation of gases, vapors, aerosols, and mixtures of these can cause a wide range of adverse health effects, ranging from simple irritation to systemic diseases. Despite significant achievements in the risk assessment of chemicals, the toxicological database, particularly for industrial chemicals, remains limited. Considering there are approximately 80,000 chemicals in commerce, and an extremely large number of chemical mixtures, in vivo testing of this large number is unachievable from both economical and practical perspectives. While in vitro methods are capable of rapidly providing toxicity information, regulatory agencies in general are still cautious about the replacement of whole-animal methods with new in vitro techniques. Although studying the toxic effects of inhaled chemicals is a complex subject, recent studies demonstrate that in vitro methods may have significant potential for assessing the toxicity of airborne contaminants. In this review, current toxicity test methods for risk evaluation of industrial chemicals and airborne contaminants are presented. To evaluate the potential applications of in vitro methods for studying respiratory toxicity, more recent models developed for toxicity testing of airborne contaminants are discussed.

Aerosols↗

Modeling acute and chronic toxicity of nonpolar narcotic chemicals and mixtures to Ceriodaphnia dubia.

The response of the daphnid Ceriodaphnia dubia to six widely used industrial chemicals acting through nonpolar narcosis and a mixture was determined. Toxicological effect levels were based on reasonably steady-state, measured concentrations. Reproductive IC50S were 149 microM benzene, 82 microM trichloroethylene, 35 microM toluene, 31 microM ethylbenzene, 26 microM m-xylene, and 4 microM tetrachloroethylene. A QSAR describing 2-day LC50S as a function of log Kow accounted for 90.97% of the variation in response across chemical. A similar QSAR for chronic effects on reproduction accounted for 78.92%. Mixtures of benzene, trichloroethylene, and toluene had effects at concentrations below their individual LOELs. Observed effects of 20/24 mixtures tested fell within the 95% prediction interval for a concentration-addition model of joint action derived from tests with individual components. However, the observed response differed significantly from the predictive relationship. In general, the predictive relationship overestimated mixture toxicity. Fitted relationships reduced observed error by as much as 82% compared to the predictive model.

Animals↗

Quantitative structure-activity relationship models correctly predict the toxic and aneuploidizing properties of six halogenated methanes in Aspergillus nidulans.

In a previous study, the relationships between the chemical structure and the ability of 35 chlorinated aliphatic hydrocarbons to induce aneuploidy and toxicity in Aspergillus nidulans were analyzed. Quantitative structure-activity relationships (QSAR) were defined for each of the biological activities under study: ARR (the dose able to block mitotic growth), D37 (the dose with 37% of survival) and LEC (the lowest efficient concentration in aneuploidy induction). In this study, these QSAR equations were used to predict the toxic and genetic activity of a further six chemicals, not included in the previous data base: bromotrichloromethane, bromoform, bromochloromethane, bromodichloromethane, dibromochloromethane and dibromochlorofluoromethane. Their ARR, D37 and LEC values were measured, and were in agreement with the predicted values, with correlation coefficients around 0.99. Furthermore, the QSAR model, which had previously been developed to discriminate between aneugenic and inactive halogenated hydrocarbons, correctly predicted the aneugenic activity of five out of six methanes. These correct predictions confirmed the validity of our QSAR model, according to which the induction of aneuploidy in A. nidulans depends on both the electrophilic and steric properties of the chemicals, whereas toxicity mainly depends on steric factors.

Aneuploidy↗

Diabetes enhances lipopolysaccharide-induced cardiac toxicity in the mouse model.

Diabetic patients have a higher rate of mortality from sepsis than do their nondiabetic septic counterparts. The hypothesis in this study is that chronic diabetes may make cardiovascular systems more sensitive to septicemia. To test this hypothesis, the authors investigated the effect of diabetes on endotoxin- induced cardiac toxicity. Diabetes was induced in FVB mice by injecting a single dose (150 mg/kg) of streptozotocin. Two months after streptozotocin treatment, the diabetic mice were treated with lipopolysaccharide by intraperitoneal injection at 2 mg/kg. Cardiac toxicity was evaluated by measuring levels of serum cardiac enzymes and cardiac morphology at 1 h, 4.5 h, and 24 h after lipopolysaccharide treatment. Serum and cardiac tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay methods at 1 h and 4.5 h after lipopolysaccharide treatment. Lipopolysaccharide treatment did not significantly affect the diabetic manifestations, including decreased body weight gain and increased glycated hemoglobin and serum triglyceride levels. However, diabetes significantly enhanced lipopolysaccharide-induced cardiac toxicity, which was demonstrated by significant increases in the levels of cardiac enzymes such as creatine phosphokinase and troponin T, abnormal morphological changes examined under light microscope with hematoxylin and eosin staining, and oxidative damage to proteins detected by 3-nitrotyrosine staining. Lipopolysaccharide treatment significantly increased serum and cardiac TNF-alpha and IL-6 concentrations. Diabetes did not alter the effect of lipopolysaccharide on serum and cardiac TNF-alpha elevation, but it significantly enhanced lipopolysaccharideinduced cardiac IL-6 production. These results suggest that diabetes significantly enhances endotoxin-induced cardiac toxicity, possibly through mechanisms that involve inflammatory/acute-phase cytokines.

Animals↗

Preclinical pharmacokinetics: an approach towards safer and efficacious drugs.

Lack of efficacy and toxicity are considered to be major reasons for drug failures and pharmacokinetics governs them to a large extent. Compound with favorable pharmacokinetics is more likely to be efficacious and safe. Therefore, the preclinical pharmacokinetic evaluation should be comprehensive enough to ensure that compounds do not fail in the clinic. Preclinical ADME screening facilitates early elimination of weak candidates and directs the entire focus of the drug development program towards fewer potential lead candidates. Hence, it is mandatory that the pre-clinical candidates are subjected to as many possible reality checks. Reliance on in-vitro tests should be minimized because they do not represent the real physiological environment but rather slow down the pace of a drug discovery program. Compounds can be straight away subjected to in-vivo high throughput screens such as cassette dosing, cassette analysis or rapid rat screen etc. Candidates with the desired in-vivo pharmacokinetic profile may be further profiled in-vitro, using assays such as metabolic stability, reaction phenotyping, CYP-450 inhibition and induction, plasma protein binding etc. in human microsomes, human recombinant CYP-450 enzymes and human plasma. This also provides an early indication of whether the compound which worked in animals would work in human as well. In-vitro metabolic stability profile is a qualitative as well as quantitative comparison of metabolism of a compound in human and animal models. It helps in identifying the right model for toxicity studies. Extensive metabolism is generally considered a liability as it limits the systemic exposure and shortens the half-life of a compound. Several strategies such as reduction of lipophilicity, modification and / or blocking of metabolically soft spots and use of enzyme inhibitors; have been developed to combat metabolism. In spite of several concerns, the fact that active metabolites of several marketed drugs have been developed as drugs with better efficacy, safety and pharmacokinetics profile; cannot be denied. Therefore, instead of considering metabolic instability a liability it can be exploited as a tool for discovering better drugs. It is equally important to identify the metabolic pathways of the drug candidates by conducting in-vitro CYP450 reaction phenotyping assays. The identification of drug metabolizing enzymes involved in the major metabolic pathways of a compound helps in predicting the probable drug-drug interactions in human. Compounds with more than one metabolic pathway have less likelihood of clinically significant drug interactions. In-vitro CYP450 inhibition and induction screens are used to evaluate the potential of compound towards drug - drug interactions and the most prone candidates may either be discarded or taken ahead with a caution. It is known that only unbound drug is pharmacologically active and therefore the assessment of bound fraction by the estimation of plasma protein binding of a compound is another important parameter to be explored in-vitro. In addition to the process of 'weeding out' weak candidates early in the drug discovery process, it is equally important to identify the probable causes of poor ADME exhibited by some compounds as this information is useful to medicinal chemists for improving upon backbones that exhibit un favorable pharmacokinetic profile. Toxicity study is the foundation of an INDA (Investigational new drug application) and therefore, the final selection of a compound can be performed only after proper toxicological evaluation in animal models. Toxicokinetics forms an integral part of toxicity study and is used to assess the exposure of candidates in toxicity models and correlate the drug levels in blood and various tissues with the toxicological findings. Although in-vivo screening of compounds in animal models and in-vitro assays in human recombinant CYP-450 enzymes help in drug candidate selection, both approaches have their own limitations. There is no certainty that the selected candidates will exhibit the desired target PK profile in human and real human PK remains suspense until the compound enters Phase-1 clinical trial. The recognition of human micro dosing, (HMD) by medicines and healthcare products regulatory agency (MHRA) and European agency for evaluation of medicinal products [EMEA] is a stepping stone in the direction of obtaining human PK data early in the preclinical stage. This would gradually shift the focus of early drug development away from animal studies directly towards safe and ethical studies in human yielding more relevant and reliable pharmacokinetic data. HMD would provide an answer to the growing public demand for a reduction in the use of animals for pharmaceutical development.

Animals↗

Synthetic GPI as a candidate anti-toxic vaccine in a model of malaria.

The malaria parasite Plasmodium falciparum infects 5-10% of the world's population and kills two million people annually. Fatalities are thought to result in part from pathological reactions initiated by a malarial toxin. Glycosylphosphatidylinositol (GPI) originating from the parasite has the properties predicted of a toxin; however, a requirement for toxins in general and GPI in particular in malarial pathogenesis and fatality remains unproven. As anti-toxic vaccines can be highly effective public health tools, we sought to determine whether anti-GPI vaccination could prevent pathology and fatalities in the Plasmodium berghei/rodent model of severe malaria. The P. falciparum GPI glycan of the sequence NH(2)-CH(2)-CH(2)-PO(4)-(Man alpha 1-2)6Man alpha 1-2Man alpha 1-6Man alpha 1-4GlcNH(2)alpha 1-6myo-inositol-1,2-cyclic-phosphate was chemically synthesized, conjugated to carriers, and used to immunize mice. Recipients were substantially protected against malarial acidosis, pulmonary oedema, cerebral syndrome and fatality. Anti-GPI antibodies neutralized pro-inflammatory activity by P. falciparum in vitro. Thus, we show that GPI is a significant pro-inflammatory endotoxin of parasitic origin, and that several disease parameters in malarious mice are toxin-dependent. GPI may contribute to pathogenesis and fatalities in humans. Synthetic GPI is therefore a prototype carbohydrate anti-toxic vaccine against malaria.

Acidosis↗

Fumonisin toxicity in a transgenic mouse model lacking the mdr1a/1b P-glycoprotein genes.

The toxicity of fumonisin B(1) (FB(1)) was investigated in male mdr1a/1b double knockout (MDRK) mice, lacking the drug-transporting P-glycoproteins. These transgenic animals are deficient in their blood:brain barrier and accumulate different drugs in brain and other tissues. The MDRK and their wild-type counterparts, FVB mice, were injected subcutaneously with 2.25 mg/kg per day of FB(1) for 5 days and sampled one day after the last treatment in a protocol that has resulted in marked hepatic and renal damage in other strains. FB(1) caused liver enlargement in both FVB and MDRK. Hematological parameters were not affected in either strain. Plasma levels of alanine aminotransferase and aspartate aminotransferase, measures of liver damage, were increased by FB(1) in both FVB and MDRK mice. Histopathological evaluation of liver corroborated this finding. Kidney lesions were induced by FB(1) in both types of mice. Concentrations of free sphingosine and sphinganine increased in liver and kidney of both strains after the FB(1) treatment, although the increase in liver sphingoid bases was half as much in MDRK as compared to FVB. The levels of sphinganine-containing complex sphingolipids were increased in kidney. The levels of sphingosine-containing complex sphingolipids in kidney were unaffected by FB(1) treatment but were significantly lower in control MDRK than in FVB mice. The levels of neurotransmitters and their metabolites were similarly affected in both strains by FB(1), suggesting no influence of disrupted blood:brain barrier on FB(1)-induced neurotoxicity. In both strains, the liver mRNA for tumor necrosis factor alpha was increased; however, the increase was statistically significant only in FVB. It was apparent that mice deficient in P-glycoprotein do not exhibit greater sensitivity to FB(1), the cellular or brain transport of FB(1) appears to be independent of this multidrug transporting system.

Journal Article↗

[Activation of free radicals reaction and changes in the state of antioxidant protection in blood in toxic experimental influenza infection].

The paper presents an experimental model of toxic influenza infection. The toxic form of influenza was shown to result in the activation of free radical processes accompanied by the accumulation of both lipid peroxidation products and methemoglobin and the decrease of alpha-tocopherol in erythrocytes, by the accumulation of NO. and nitrizyl complexes of heme iron in the blood. The activation of free radical processes was followed by the stimulation of antioxidant system in the blood. Thus, there was an increase of both superoxide dismutase activity in erythrocytes and ceruloplasmin content in the blood. The data obtained support the important role of the active products of free radical processes in the development of toxicosis under acute virus infections.

Acute Disease↗