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PubMed2002

An investigation of new toxicity test method performance in validation studies: 1. Toxicity test methods that have predictive capacity no greater than chance.

An approach commonly used to measure new toxicity test method (NTM) performance in validation studies is to divide toxicity results into positive and negative classifications, and the identify true positive (TP), true negative (TN), false positive (FP) and false negative (FN) results. After this step is completed, the contingent probability statistics (CPS), sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) are calculated. Although these statistics are widely used and often the only statistics used to assess the performance of toxicity test methods, there is little specific guidance in the validation literature on what values for these statistics indicate adequate performance. The purpose of this study was to begin developing data-based answers to this question by characterizing the CPS obtained from an NTM whose data have a completely random association with a reference test method (RTM). Determining the CPS of this worst-case scenario is useful because it provides a lower baseline from which the performance of an NTM can be judged in future validation studies. It also provides an indication of relationships in the CPS that help identify random or near-random relationships in the data. The results from this study of randomly associated tests show that the values obtained for the statistics vary significantly depending on the cut-offs chosen, that high values can be obtained for individual statistics, and that the different measures cannot be considered independently when evaluating the performance of an NTM. When the association between results of an NTM and RTM is random the sum of the complementary pairs of statistics (sensitivity + specificity, NPV + PPV) is approximately 1, and the prevalence (i.e., the proportion of toxic chemicals in the population of chemicals) and PPV are equal. Given that combinations of high sensitivity-low specificity or low specificity-high sensitivity (i.e., the sum of the sensitivity and specificity equal to approximately 1) indicate lack of predictive capacity, an NTM having these performance characteristics should be considered no better for predicting toxicity than by chance alone.

False Negative Reactions↗

PubMed2000

Isolation of bacteria from toxic dinoflagellate Alexandrium minutum and their effects on algae toxicity.

Attempts were made to isolate the bacteria from toxic dinoflagellate Alexandrium minutum T1 and to study the effect of these bacteria on the growth and toxicity of A. minutum T1. It was found that intracellular bacterial species including Pasteurella haemolytica, Pseudomonas vesicularis, and Sphingomonas sp., and extracellular bacterial species including Pasteurolla pneumotropica, Morganella wisconsensis, Flavobacterium oryzihabitans, Pseudomonas pseudomallei, and Sphingomonas sp. All of them were cultured and determined to have non-PSP-producing ability. The maximum cell number of A. minutum cultured without isolated bacteria was higher than that cultured with isolated bacteria. The total toxicity of A. minutum cultured with bacteria was similar to that of A. minutum T1 cultured without bacteria from lag phase to stationary phase, but it was lower after stationary phase. The growth of A. minutum T1 cultured without antibiotics was also better than that cultured with antibiotics. The total toxicity of A. minutum cultured without antibiotics was higher than that of A. minutum cultured with antibiotics. However, the cell toxicity of A. minutum did not decrease even if the culture medium was added with antibiotics.

Animals↗

PubMed1994

Aminoglycoside toxicity in the treatment of endophthalmitis. The Aminoglycoside Toxicity Study Group.

OBJECTIVE AND METHODS: Intravitreous aminoglycosides are widely used for the treatment and prophylaxis of endophthalmitis. Because the toxicity of 0.4 mg of gentamicin sulfate is well documented, many surgeons now use amikacin sulfate or low-dose gentamicin to reduce the risk of macular infarction. A survey of retinal specialists has suggested that amikacin or low-dose gentamicin can also cause macular toxic side effects. To further investigate this issue, the critical details of the case histories, findings, and course of 13 patients who received intravitreous injections of 0.2 to 0.4 mg of amikacin sulfate or 0.1 to 0.2 mg of gentamicin sulfate for prophylaxis or treatment of endophthalmitis are summarized. For several patients, complete case histories and a fluorescein angiogram are provided. RESULTS: These cases suggest that amikacin and low-dose gentamicin, similar to gentamicin sulfate at a dose of 0.4 mg, can cause macular infarction. The causative dose cannot be ascertained in any of the cases, but doses were prepared by hospital pharmacists using typewritten protocols, a practice that helps to prevent dilution errors. Several of these cases differ from previously reported cases of aminoglycoside toxicity in that the involvement of the macula was quite discrete. Most of the patients suffered severe visual loss, but two patients, in whom most of the nonperfusion was adjacent to the macula and in whom some of the perifoveal capillaries were spared, recovered 20/50 visual acuity. CONCLUSIONS: These cases emphasize the potential hazards of the intravitreous use of aminoglycosides. A toxic reaction can occur even when injection of low doses is intended and precautions are made to avoid dilution errors. A localized increase in concentration in dependent areas of the retina may play a role in aminoglycoside toxicity. If some of the perifoveal capillaries are spared, retention of some central vision is possible. Consideration should be given to substituting ceftazidime for aminoglycosides for the treatment and prophylaxis of endophthalmitis.

Aged↗

PubMed1987

Application of the preliminary developmental toxicity screen for chemical hazard identification under the Toxic Substances Control Act.

The Office of Toxic Substances (OTS) within the U.S. Environmental Protection Agency (EPA) is authorized to carry forth the mandates of the Toxic Substances Control Act (TSCA). Included among the provisions of TSCA are the development of requirements for testing of "new" and "existing" chemicals that may present an unreasonable risk of injury to health or the environment. There are over 63,000 "existing" chemicals on the TSCA inventory, and EPA in recent years has been receiving an average of over 1,300 submissions for "new" chemicals a year. Since it is illogical and unrealistic to expect that all of these chemicals should be subjected to detailed testing for all potential adverse health and environmental effects, OTS views screening assays as highly useful tools to assign priorities to chemicals for further testing according to standard methodologies. The Chernoff/Kavlock assay (preliminary developmental toxicity screen) was specifically developed to address the need for a developmental toxicity assay to prioritize for further testing the large number of "new" and "existing" chemicals. OTS has been involved in seeking the development of data through the preliminary developmental toxicity screen for purposes of validating the screen and to obtain critical data necessary for evaluating chemicals. OTS believes that the screen has a role in the risk assessment process and has developed a testing protocol, which is included along with other OTS test guidelines; has provided internal guidance on when the screen may be recommended; and has discussed how the data may be applied in prioritizing chemicals for further study.

Animals↗

PubMed1994

The relevance of aquatic organisms' lipid content to the toxicity of lipophilic chemicals: toxicity of lindane to different fish species.

The acute toxicity (48-hr LC50) of lindane (gamma-HCH) to 16 fish species, belonging to eight families, ranges from 22 to 900 micrograms/liter (mean: 150 micrograms/liter). A significant positive linear relationship between the lipid content (% on a wet weight basis) of the fishes and their toxicity to gamma-HCH was found. If the toxicity is referred to 1% lipid, 48-hr LC50 values range between 13.2 and 32 micrograms/liter, and thus the coefficient of variation of the mean is reduced from 139 to 22%. It is concluded that the lipids of aquatic organisms serve as a protective reservoir against the toxic effects of lindane and other lipophilic, relatively persistent organic chemicals, because they are bioconcentrated mainly in the body lipids. Therefore, in organisms with high lipid content, only a relatively small fraction of the hydrophobic chemical can reach target organs (nerves, liver, etc.) and/or receptors. For comparing toxicity data of organic chemicals to aquatic organisms, the total lipid content of the organisms must be considered. The results of this investigation are important in comparative environmental toxicology for risk assessment of freshwater and marine organisms.

Animals↗

PubMed1996

Use of a miniaturized test system for determining acute toxicity of toxicity identification evaluation fractions.

A miniaturized test system was developed and used to determine the acute toxicity of effluent fractions separated by HPLC to Daphnia magna and Pimephales promelas. The miniaturized test system consists of exposing test organisms in 1 ml of test solution using 48-well microtiter plates for the test vessels. Several factors were investigated to determine the acceptability of this test system. These factors included organism biomass to test solution ratio, toxicity of the microtiter plates to the organisms, dissolved oxygen in the test solution, partitioning of the test chemicals to the walls of the test vessels, and dilution of the test solution when the organisms are transferred. Toxicity of four reference chemicals to D. magna and P. promelas was also determined using the miniaturized test systems. It was concluded that the test system could be miniaturized and still provide results comparable to those obtained when standard U.S. EPA test procedures were used. The major benefit of using the miniaturized test system is that less solution is required for conducting a toxicity test. This becomes important when only a small amount of test solution is available, as might occur during a toxicity identification evaluation, after an effluent has been fractionated by HPLC. Other benefits include less space required to conduct a test, less time necessary to prepare test solutions, and a reduced volume of waste for disposal.

Animals↗

PubMed1997

Sequence of toxic events in arsine-induced hemolysis in vitro: implications for the mechanism of toxicity in human erythrocytes.

Arsine, the hydride of arsenic (AsH3), is the most acutely toxic form of arsenic, causing rapid and severe hemolysis upon exposure. The mechanism of action is not known, and there are few detailed investigations of the toxicity in a controlled system. To examine arsine hemolysis and understand the importance of various toxic responses, human erythrocytes were incubated with arsine in vitro, and markers of toxicity were determined as a function of time. The earliest indicators of damage were changes in sodium and potassium levels. Within 5 min incubation with 1 mm arsine, the cells lost volume control, manifested by leakage of potassium, influx of sodium, and increases in hematocrit. Arsine did not, however, significantly alter ATP levels nor inhibit ATPases. These changes were followed by profound disturbances in membrane ultrastructure (examined by light and electron microscopy). By 10 min, significant numbers of damaged cells formed, and their numbers increased over time. These events preceded hemolysis, which was not significant until 30 min. It has been proposed that arsine interacts with hemoglobin to form toxic hemoglobin oxidation products, and this was also investigated as a potential cause of hemolysis. Essentially on contact with arsine, methemoglobin was formed but only reached 2-3% of the total cellular hemoglobin and remained unchanged for up to 90 min. There was no evidence that further oxidation products (hemin and Heinz bodies) were formed in this system. Based on these observations, hemolysis appears to be dependent on membrane disruption by a mechanism other than hemoglobin oxidation.

Adult↗

PubMed2001

Structure toxicity relationships--how useful are they in predicting toxicities of new drugs?

This chapter provides just a few newer examples of structural moieties found in drugs that have been associated with reactive metabolite formation and toxicities. For a discussion of several other structures in drugs that undergo metabolic activation to reactive intermediates, the reader is directed to previous volumes in this series and other chapters in this book, as well as a previous condensed review (Nelson, 1982). Since that review, some new knowledge allows us to better predict that some structural moieties are more likely than others to form drug reactive metabolites that may be involved in causing toxic effects in humans. For example, most aniline-, thiophene-, and nitroaromatic-containing drugs have had a relatively high incidence of adverse effects, and it would be prudent in the drug discovery process to avoid these substructures if possible. However, as illustrated by the case of olanzapine, these structures may be important for potent activity, and could therefore be beneficial in some cases. The glitazones represent a new class of drugs with a unique thiazolidinedione structure. This raises two important points. First, it demonstrates how limited our knowledge base is in regard to structure toxicity relationships when new structures are introduced. Our approaches must be very empirical and are far from quantitative for the reasons outlined in the introduction. Secondly, the glitazones point out the importance of benefit/risk considerations. This was a new structural class of drugs with a unique spectrum of action that is very beneficial in the treatment of a major disease. Despite some suspected risk of toxicity, based on early trials, troglitazone was approved for use with careful monitoring. This author believes that was the right decision, as was the decision to withdraw the drug when the risk became unacceptable, especially with the introduction of safer alternatives. If this were just another NSAID (e.g., bromfenac), there would be little reason for approval. In summary, as I pointed out previously (Nelson, 1982), with our limited knowledge of structure toxicity relationships, we can only make reasonable judgments as to risk assessment of a new drug in humans, and hope that we neither release a dangerous chemical entity nor, as importantly, abort an effective one.

Analgesics↗

PubMed2000

Studies of aminochrome toxicity in a mouse derived neuronal cell line: is this toxicity mediated via glutamate transmission?

Aminochrome was found to be toxic in a mouse-derived neuronal cell line (CNh). The effect was concentration dependent (10-150microM). The issue whether aminochrome toxicity involves glutamate transmission was studied with several glutamate receptors antagonists. Incubation of the cells with aminochrome (150microM) in the presence of 100microM of the AMPA antagonist, NBQX resulted in an increase of cell survival, from 52 to 73%. However, this protective effect did not seem to be related to activation of ionotropic glutamate receptors since incubation of CNh cells with 200microM of glutamate resulted in only 10% decrease of cell survival. However, NBQX was found to inhibit in vitro the autoxidation process. One hundred microM AP-5 did not have any effect on aminochrome toxicity. The toxic effect of aminochrome on CNh cells seems to be dependent of extracellular activation since addition of dicoumarol, a specific inhibitor of DT-diaphorase, did not affect that toxicity, which can be explained perhaps by a lack of a transport system for aminochrome into the CNh cells.

Animals↗

PubMed1991

Interpreting aquatic toxicity QSARs: the significance of toxicant body residues at the pharmacologic endpoint.

Aquatic QSAR investigations employ bioassay data where a biological response is associated with a toxicant concentration in the exposure water. Although convenient this ignores the fundamental principle that the response is more closely related to an amount present in the organism. This problem has been examined using acute toxicity and bioconcentration QSARs employing log Kow as the molecular descriptor. Combining these QSAR relationships enables estimates of the amount of toxicant in organisms to be made. For acute narcosis (50% mortality) the toxicant level in the hydrophobic (lipid) phase of an exposed organism is, as a first approximation, constant at approximately 50 mmol l-1 of lipid. For the acute toxicity of a variety of hydrophobic narcotic organics examined by US EPA-Duluth in tests with fathead minnows, this corresponds to a whole-body residue of about 4 mmol kg-1. Although the level in the hydrophobic phase remains constant, for hydrophilic chemicals (log Kow less than 1.5) the contribution of the hydrophilic (water) phase of the organism dominates and total body residues should be similar to the respective threshold LC50s. This has important implications in simple pharmacokinetic modelling and in interpreting residue levels in organisms collected in environmental monitoring studies.

Animals↗

PubMed1992

Role of maternal toxicity in assessing developmental toxicity in animals: a discussion.

The belief that any drug or chemical, when administered at a high enough dose, can be expected to produce fetal malformations is not consistent with the facts. However, the stress associated with maternally toxic doses can be expected to result in associated, often transient, fetal abnormalities that may not be the result of deviant organogenesis. Sometimes the toxicity toward the pregnant animal, including her embryos/fetuses since they are hardly in a sanctuary, is severe enough to result in resorption of the embryo or abortion of the fetus. Thus, it is possible that the embryolethality and other indications of developmental toxicity, produced by some drugs and chemicals, may be the result of a mechanism(s) other than selective toxicity toward the embryo. Also, some test materials have been shown to affect maternal homeostasis, thereby disrupting support to the embryo, without causing significant overt toxicity to the embryo or dam; e.g., the endocrine system of the dam is altered. Routine testing has thus far revealed a relatively limited number of true teratogens, although a large number of drugs and chemicals have resulted in fetal effects such as developmental variations when administered at doses that approach lethal levels. Such effects on the fetus should be expected when the maternal animals are stressed by the high dosages usually employed. A better understanding of the etiology and biological relevance of the embryo/fetal deviations often seen in developmental toxicology studies might help to avoid the sometimes unjustified withholding of potentially useful drugs and chemicals from the marketplace.

Abnormalities, Drug-Induced↗

PubMed1988

Comparative toxicities of the naturally occurring nitrile 1-cyano-3,4-epithiobutane and the synthetic nitrile n-valeronitrile in rats: differences in target organs, metabolism and toxic mechanisms.

Toxic but sublethal oral doses of 125 mg/kg (1.1 mmol/kg) of the cruciferous nitrile, 1-cyano-3,4-epithiobutane (CEB), or 175 mg/kg (2.1 mmol/kg) of its synthetic saturated analogue, n-valeronitrile (VN), were given by gavage to male CDF (F-344/CrlBr) rats once daily for 1, 2 or 3 days, in order to compare target tissues and to observe structure-activity relationships between the nitriles. CEB-induced changes included degeneration and necrosis of the pars recta of the renal proximal tubules, ulceration and necrosis in the forestomach, a mild increase (4.5-fold) in daily urinary thiocyanate (SCN-) excretion (only in rats treated for 3 days) and 1.5- to 2.4-fold increases in hepatic and pancreatic non-protein thiol (RSH) concentrations (in all CEB-treated groups). In VN-treated rats, there were no consistent histological changes but 95- to 170-fold increases in daily urinary SCN- excretion, delayed clinical signs of cyanide toxicity and minimal effects on tissue RSH concentrations. These results indicate different toxic mechanisms for VN and CEB. The nephrotoxic effects of CEB were very similar to those of 1-cyano-2-hydroxy-3,4-epithiobutane, suggesting a role for the epithio group in the nephrotoxicity of these nitriles. The relatively low SCN- excretion in CEB-treated rats also suggested that cyanide played only a minimal role in CEB toxicity, while the high SCN- excretion, clinical signs of cyanide poisoning and lack of histological changes imply a greater role for metabolically-derived cyanide in VN toxicity. The enhancement of tissue RSH by CEB treatment with indications of enhanced tissue glutathione concentrations suggested the involvement of glutathione in the detoxication of CEB and/or its reactive metabolites.

Animals↗

PubMedDate not supplied

Pulmonary toxicity of 2-methylnaphthalene: lack of a relationship between toxicity, dihydrodiol formation and irreversible binding to cellular macromolecules in DBA/2J mice.

Intraperitoneal doses of 2-methylnaphthalene (2-MN) have been shown to cause pulmonary toxicity in DBA/2J mice. Pretreatment with the monooxygenase inducers sodium phenobarbital and 3-methylcholanthrene (3-MC) failed to protect the DBA/2J mice from the toxic effect of 2-methylnaphthalene. Pretreatment of DBA/2J mice with the monooxygenase inhibitors, SKF 525-A and piperonyl butoxide also failed to enhance or attentuate the pulmonary lesions. Pulmonary and hepatic microsomes from DBA/2J mice metabolized 2-methylnaphthalene to three dihydrodiols, 2-naphthyl alcohol and other unidentified metabolites. Kidney microsomes produced 2-naphthyl alcohol but no detectable dihydrodiols. In comparison to control animals, hepatic microsomes from animals pretreated with sodium phenobarbital produced more of the least polar dihydrodiol, while amounts of the other two dihydrodiols were unaffected. 3-Methylcholanthrene, piperonyl butoxide and diethylmaleate failed to affect dihydrodiol formation in both pulmonary and hepatic microsomes. After the administration of a lung toxic dose (400 mg/kg, i.p.) of 2-MN, irreversible binding was highest in the liver, followed by the kidney, the lung and lastly skeletal muscle. Of the pretreatments given to the mice, only phenobarbital demonstrated a significant effect, and this elevation was apparent only in the liver. A pulmonary toxic dose of 2-MN (400 mg/kg, i.p.) administered to DBA/2J mice significantly depleted reduced GSH in the liver and lung and to a lesser extent, in the kidney. There appeared no good correlation between the pulmonary toxicity of 2-MN-dihydrodiol and/or alcohol formation or the in vivo irreversible binding to macromolecules. These results are compared with those reported previously in C57BL/6J mice.

Animals↗

PubMed1981

Toxicity of endosulfan and manganese chloride: cumulative toxicity rating.

There has been, in general, no accepted comparable way to express the effects of repeated doses. This study was designed to provide information on cumulative toxicity of manganese chloride (MnCl2), endosulfan, and a mixture of these compounds and to suggest cumulative toxicity rating. Male mice were given the test compound i.p. 6 days/week for a minimum for 10 weeks and until the cumulative LD50 remained constant for 3 consecutive weeks. Using a ratio between a single dose and weekly cumulative LD50 (CLD50), cumulative toxic factors (CTF) were determined. The CTF for weeks 1-13 for MnCl2 ranged from 0 to 3.48; endosulfan LD50 and CLD50 values for a mixture of MnCl2 and endosulfan were higher than the expected values, indicating a greatly reduced toxicity of a mixture, when given either in a single dose or repeated doses. Using the CLD50 criterion as laid down in this study, the cumulative toxicity rating, class 1 to 6, has been suggested so as to have a comparative assessment of th cumulative potential of several compounds.

Animals↗

PubMed1995

Toxic equivalency factors do not predict the acute toxicities of dioxins in rats.

Risk evaluation of complex environmental mixtures of polychlorinated dibenzo-p-dioxins and related halogenated aromatic hydrocarbons (polychlorinated dibenzofurans, azo- and azoxybenzenes, naphthalenes and some of the biphenyls) is currently carried out by measuring the concentration of each congener in the mixture and then multiplying every figure by its specific constant, toxic equivalency factor (TEF). All congeners are thought to produce highly similar effects albeit at different doses, and the TEFs are believed to represent the potencies of the congeners relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), considered the most toxic derivative of this class of environmental contaminants. Here we compared the acute toxicities of TCDD, 1,2,3,7,8-penta-, 1,2,3,4,7,8-hexa- and 1,2,3,4,6,7,8-heptachloro-dibenzo-p-dioxin in the most TCDD-susceptible (Long-Evans Turku AB; L-E) and the most TCDD-resistant (Han/Wistar kuopio; H/W) rat strain. While L-E rats exhibited the expected rank order of sensitivities to the four dioxins, the higher chlorinated dioxins were more toxic than TCDD (in terms of acute lethality) to H/W rats, with the hexachlorodioxin showing the greatest potency. Even if the doses were adjusted according to the LD50 values, both biochemical and morphological effects elicited by the dioxins turned out to depend, often critically, on strain, congener or the interaction of these two determinants. These findings demonstrate that the dioxins have distinct profiles of acute toxicities and underscore the importance of response and test organism in defining the TEFs.

Animals↗

PubMed2004

Enzymatic activity of toxic and non-toxic type 2 ribosome-inactivating proteins.

Ribosome-inactivating proteins (RIPs) display adenine polynucleotide glycosylase activity on different nucleic acid substrates, which at the ribosomal level is responsible for the arrest of protein synthesis. Some type 2 RIPs, namely ricin and related proteins, are extremely toxic to mammalian cells and animals whilst other type 2 RIPs (non-toxic type 2 RIPs) display three to four logs less toxicity. We studied whether a correlation exists between toxicity on cells and enzymatic activity on nucleic acids. All type 2 RIPs differ in their depurinating activity on the different substrates with differences of up to one to two logs. The toxicity of type 2 RIPs is independent of their enzymatic activity on nucleic acids or on ribosomes.

Abrin↗

PubMed2001

Impact of a toxic and a non-toxic strain of Microcystis aeruginosa on the crayfish Procambarus clarkii.

The occurrence of cyanobacteria in many water bodies where crayfish such as Procambarus clarkii are abundant leads to the possibility of toxin accumulation and food chain transfer. This paper describes the accumulation and depuration of microcystins from a microcystin and a non-microcystin producing strain of Microcystis aeruginosa, on the survivorship, growth and nutritional status of P. clarkii. Crayfish larvae were resistant to cyanobacteria and their toxins, surviving cyanobacteria densities during acute exposures. Juvenile crayfish tolerated toxic cyanobacteria better than non-toxic ones. This effect was also observed when analysing nutritional status of crayfish fed toxic and non-toxic cyanobacteria with the former having better lipid and protein contents than those fed non-toxic Microcystis. P. clarkii accumulated up to 2.9 microg MCYST/dry crayfish weight and the depuration pattern was similar to that observed for mussels by other authors. Due to the fact that the major part of the toxin is accumulated in the intestine and in the hepatopancreas, there is no significant risk in terms of human health if these parts are removed prior to crayfish consumption. Nevertheless, their use in dairy food and the possible transference of toxins along food chains should not be disregarded.

Animals↗

PubMed2002

Acute toxicity of chlorophenols to earthworms using a simple paper contact method and comparison with toxicities to fresh water organisms.

An acute toxicity test of chlorophenols on earthworms (Eisenia fetida) was performed using a simple paper contact method proposed by OECD testing guideline no. 207, that were applied as an earthworm toxicity test. The median lethal concentration, EC50, had significant correlation with logP(ow) (1-octanol/water partition coefficient) of the chemicals. The toxicity of chlorophenols on E. fetida was compared with toxicities for other species: an algae (Selenostrum capricornutum), a crustacean (Daphnia magna), and a fish (Oryzias latipes). It was found that the toxicity of chlorophenols was almost same for E. fetida and for fresh water organisms. These results suggest the possibility of drawing correlations between the effects of pollutants on living things in different environments, fresh water and soil.

Animals↗