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At least 721 records · Page 40Linked to original sources
PubMed2003

Viscoanesthesia. Part I: toxicity to corneal endothelial cells in a rabbit model.

PURPOSE: To evaluate the toxicity of a solution combining sodium hyaluronate 1.5% with lidocaine (0.5%, 1.0%, or 1.65%) to the rabbit corneal endothelium. SETTING: Center for Research on Ocular Therapeutics and Biodevices, Storm Eye Institute, Medical University of South Carolina, Charleston, South Carolina, USA. METHODS: Each rabbit cornea was excised, and the endothelium was exposed to 1 of the following solutions for 20 minutes: viscoanesthetic solution (0.5%, 1.0%, or 1.65% lidocaine in sodium hyaluronate 1.5%; 5 corneas each), sodium hyaluronate 1.5% (n = 5), balanced salt solution (BSS(R)) (n = 5), mitomycin-C 0.02% (n = 2), dextran 15% (n = 2), or distilled water (n = 2). The endothelium was then stained with trypan blue and alizarin red. Two corneas were stained immediately after excision. Cell morphology and damage to the corneal endothelium were analyzed by microscopic examination. RESULTS: The endothelium in the corneas of the viscoanesthetic groups was comparable to that in the sodium hyaluronate 1.5% and the BSS groups and to the corneas not exposed to any solution. In some areas of the 1.0% and the 1.65% viscoanesthesia groups, the corneal endothelial cells presented irregular intercellular borders. Staining with trypan blue, which indicates cellular damage, was observed in some linear areas corresponding to corneal folds in all groups. The folds were probably caused during manipulation for corneal excision and staining. The corneal endothelium was destroyed in the mitomycin group. In the dextran and distilled-water groups, morphological alterations probably resulting from osmotic changes were observed. CONCLUSIONS: The 3 concentrations of viscoanesthetic solutions appeared to be safe to rabbit corneal endothelium.

Acetates↗
PubMed1987

Retinal toxicity of combination antiviral drugs in an animal model.

We investigated the retinal toxicity of various combinations of four antiviral agents in intravitreal injection and vitrectomy infusion solutions in the rabbit. The nontoxic concentration of each individual agent for intravitreal injection and for vitrectomy infusion has previously been described. Our results support the concept that concentrations of 200 micrograms/0.1 mL of trifluridine, 400 micrograms/0.1 mL of hydroxyacyclovir, 200 micrograms/0.1 mL of acyclovir and 30 micrograms/0.1 mL of vidarabine can be combined for intravitreal injection without toxic retinal effects. Moreover, 60 micrograms/mL of trifluridine, 20 micrograms/mL of hydroxyacyclovir, 40 micrograms/mL of acyclovir and 8 micrograms/mL of vidarabine can be combined in vitrectomy infusion solutions without retinal damage. Further study is needed to determine the full potential of such combinations.

Acyclovir↗
PubMed2026

Bacterial polar metabolites modulate β-amyloid toxicity and cholinergic dysfunction in models of Alzheimer's disease.

Alzheimer's disease is characterized by progressive neurodegeneration driven by β-amyloid (Aβ) toxicity, oxidative stress, and cholinergic dysfunction. In this study, we investigated whether polar metabolites derived from a cultivable bacterial isolate could modulate Aβ-associated neurodegenerative phenotypes in complementary experimental models. A bioactivity-guided approach identified an aqueous fraction with high antioxidant capacity in DPPH, FRAP, and ORAC assays. In a transgenic Drosophila melanogaster model expressing human Aβ, treatment with this fraction significantly reduced amyloid accumulation and attenuated neurodegenerative histopathological alterations. In human SH-SY5Y neuronal cultures, the metabolites improved cell viability under therapeutic, but not preventive, conditions following exposure to aggregated Aβ. The aqueous fraction also exhibited significant inhibitory activity against acetylcholinesterase and butyrylcholinesterase. Whole-genome sequencing assigned the bioactive isolate to the genus Providencia, with comparative genomic analyses suggesting its placement within a distinct taxonomic lineage. Metabolomic profiling by LC-ESI-MS/MS revealed a diverse set of polar metabolites, including metabolites putatively annotated based on spectral matching, previously associated with neuroprotective and cholinesterase-modulating activities. Collectively, these findings demonstrate that bacterial polar metabolites can modulate key pathological features of Alzheimer's disease, supporting their relevance for mechanistic studies of Aβ toxicity and cholinergic dysfunction.

Animals↗
PubMed2004

Serum hyaluronan and hyaluronidase: very early markers of toxic liver injury.

BACKGROUND: Dimethylnitrosamine (DMN), a potent hepatotoxin, administered to rats, provides a convenient model for toxic liver injury. Indicators of early liver injury are important clinically, for surveillance, for screening new drugs that are potentially hepatotoxic and for identifying drugs that protect against liver injury. Both cirrhosis and wound healing culminate in deposition of fibrous connective tissue and scarring. Increased hyaluronan (HA) occurs in the earliest stage of wound healing. Hyaluronidase, the enzyme that degrades hyaluronan, is also elevated whenever rapid turnover of hyaluronan occurs. We test the hypothesis that elevated levels of circulating hyaluronan and hyaluronidase could provide indicators of very early liver damage. METHODS: Dimethylnitrosamine was administered to adult male albino rats by intraperitoneal injections for 7 consecutive days. RESULTS: Increased serum hyaluronan levels observed on day 2 reached a maximum on day 4. Hyaluronidase was elevated on the first day and reached a maximum on day 2 that was 30-times control levels. Hyaluronan-specific staining in liver sections was maximal on day 7, occurring predominantly in portal triads and in sinusoidal spaces. Individual hepatocytes were slightly enlarged and contained intracellular hyaluronan, which was not evident in control sections. Though circulating hyaluronan levels had decreased after day 4, continued hyaluronan staining persisted in liver sections through day 21. Conventional indicators of liver injury, such as serum aminotransferase enzymes, did not reach a peak until day 7. Conventional gross and histopathological changes, including severe centrilobular congestion and hemorrhagic necrosis, were observed only after day 7. Both hyaluronan and hyaluronidase are indicators of very early liver damage in the dimethylnitrosamine-treated rat, occurring well before conventional indicators appear, or before overt histopathologic changes of liver damage can be seen. However, levels are increased only transiently, indicating that serial assays are necessary. CONCLUSIONS: Measures of circulating hyaluronidase activity may be used to assess liver damage.

Alanine Transaminase↗
PubMedDate not supplied

Passive protection of rabbits infected with toxic shock syndrome-associated strains of Staphylococcus aureus by monoclonal antibody to toxic shock syndrome toxin 1.

The effectiveness of passive immunization was assessed in an infection model of toxic shock syndrome (TSS) in which monoclonal antibody to TSS toxin 1 (TSST-1) was administered intravenously to rabbits. Previously implanted infection chambers were inoculated with Staphylococcus aureus strains RN4710 and D4508. The former strain carries the TSST-1 gene on plasmid pRN6201; the latter is a TSST-1-negative clinical isolate obtained from a patient with nonmenstrual TSS. Purified monoclonal antibody, MAb 8-5-7 (IgG), was administered in two doses of approximately 1.25 mg each 24 hours before and 24 hours after infection. MAb 8-5-7 provided complete protection against both the TSS-like syndrome and the mortality that occurred in unprotected rabbits infected with strain RN4710 but did not provide complete protection in rabbits infected with strain D4508; three of the five rabbits either displayed signs of illness or died despite treatment. Western-blot analyses of the extracellular proteins produced by strains RN4710 and D4508 that used MAb 8-5-7 as a probe revealed that only TSST-1 produced by RN4710 reacted with the antibody. Thus, if MAb 8-5-7 partially protected animals against infections with strain D4508, the protection appears to have been nonspecific.

Animals↗
PubMed1998

Protection of human upper respiratory tract cell lines against sulphur mustard toxicity by glutathione esters.

1. Human and animal lung cells have been used successfully to model the toxic effects of inhaled sulphur mustard (HD). The epithelia of the upper respiratory tract are, however, the primary targets of inhaled HD. The aim of this study was to assess the potential of the mono- and di-isopropyl esters of glutathione (MIPE and DIPE respectively) as cytoprotectants in the human upper respiratory tract cell lines BEAS-2B and RPMI 2650. 2. The optimal concentrations for cytoprotection were shown to be 1.0 mg/ml for both DIPE and MIPE. Both compounds were found to protect cells by pretreatment, slightly less protection was observed in cells simultaneously exposed to sulphur mustard. The greatest protection was shown where MIPE or DIPE were in in situ at the time of exposure to HD. The optimum pre-treatment times were found to be 1 h for MIPE and 2 h for DIPE. Limited protection of cells treated with MIPE or DIPE immediately following HD exposure was also demonstrated. No protection was observed if MIPE or DIPE were not administered immediately following HD exposure. 3. Results suggest that MIPE and DIPE may be effective treatments for exposure to HD by inhalation.

Cell Line↗
PubMed1987

Effects of toxic shock syndrome Staphylococcus aureus, endotoxin and tampons in a mouse model.

Synthetic tampons and toxic shock syndrome toxin-one (TSST-1)-producing strains of Staphylococcus aureus have been linked to an increased incidence of toxic shock syndrome (TSS). While recent reports attempt to define the tampon connection as the creation of an optimal environment for the production of TSST-1, the role of other factors in disease expression in an animal model remain under investigation. To understand the role of tampons and bacteria, pools of Swiss mice were inoculated with permutations of effluents from TSS strains of S. aureus and Escherichia coli grown inside tampons. Depending on tampon brand, when all 3 factors were combined mortality ranged from 20-100%. In controls inoculated with single effluents, or effluents from growth in the presence of cotton, no deaths were observed. Likewise, when hairless mice were inoculated with exotoxin, endotoxin, and tampon leachables, mortality was 100%. In the absence of any 1 component, mortality ranged from 0-40%. Lethal toxicity can be the result of enhancement, since animal death in apparent shock was observed in all pools containing the 3 components, and in all pools containing effluents of TSS S. aureus and E. coli grown in the presence of synthetic tampons, but not in their absence. A retrospective analysis of fatal vs non-fatal TSS in humans supports the hypothesis of enhancement.

Adolescent↗
PubMed2005

Acute esophageal toxicity in non-small cell lung cancer patients after high dose conformal radiotherapy.

BACKGROUND AND PURPOSE: To correlate acute esophageal toxicity with dosimetric and clinical parameters for non-small cell lung cancer (NSCLC) patients treated with radiotherapy (RT) alone or with chemo-radiotherapy (CRT). PATIENTS AND METHODS: We analyzed the data of 156 patients with medically inoperable or locally advanced NSCLC. Seventy-four patients were irradiated with high dose RT only, 45 patients with sequential CRT (Gemicitabine/Cisplatin) and 37 patients with concurrent CRT (Cisplatin daily 6 mg/m(2)). The radiation dose delivered ranged from 49.5 to 94.5 Gy (2.25-2.75 Gy per fraction) with an overall treatment time of 5-6 weeks. For all patients the maximal acute esophageal toxicity (RTOG/EORTC criteria) was scored and related to dose-volume parameters, as well as to clinical and treatment-related parameters. All parameters were tested univariable and multivariable in a binary logistic regression model. The toxicity data of a homogeneous subgroup was fitted to the Lyman-Kutcher-Burman model. RESULTS: Grade 2 acute esophageal toxicity or higher occurred in 27% (n=42) of the patient population of which nine patients developed grade 3 toxicity and one patient grade 4. All 10 patients with grade>or=3 esophageal toxicity received concurrent CRT. At multivariable analysis, the most significant clinical parameter to predict acute esophageal toxicity was the concurrent use of CRT. The most significant dosimetric parameter was the esophagus volume that received at least 35 Gy. The data of the patients who did not receive concurrent CRT were well described by the Lyman-Kutcher-Burman normal tissue complication probability model. The optimal fit of the data of non-concurrent treated patients to this model was obtained using the following values for the parameters: TD(50)=47 Gy (41-60 Gy), n=0.69 (0.18-6.3) and m=0.36 (0.25-0.55) where the numbers between brackets denote the 95% confidence interval. Acute esophageal toxicity was not significantly increased for patients treated with sequential CRT. CONCLUSION: Both concurrent CRT and the volume that receives at least 35 Gy were predictors of acute esophageal toxicity.

Acute Disease↗
PubMed2000

A rat nasal epithelial model for predicting upper respiratory tract toxicity: in vivo-in vitro correlations.

An in vitro model of the rat nasal cavity has been used to compare the responses of nasal tissues in vitro, using loss of intracellular ATP and potassium as indices of toxicity, with the pathological changes occurring following in vivo exposure to four test compounds. Turbinates were incubated in vitro with the test compounds for 4 h, for 24 h or for 4 h followed by 20 h in fresh medium. Titanium dioxide caused little or no loss of ATP in either olfactory epithelium (OE) or respiratory epithelium (RE). Sodium carbonate decreased olfactory, but not respiratory ATP, while acetic acid and 3-methylindole markedly decreased ATP in both tissues. Intracellular potassium concentrations were generally affected to a lesser degree. In vivo, no morphological changes were observed in the nasal cavity following inhalation exposure to either titanium dioxide or sodium carbonate. Inhalation of acetic acid resulted in a very focal lesion in the RE of the dorsal meatus of level 1, while administration of 3-methylindole by intraperitoneal injection caused severe degeneration of OE. In further experiments olfactory turbinates were exposed to a range of concentrations (0-100 mM) of sodium carbonate, acetic acid and 3-methylindole for 4 h and ATP concentrations determined. Concentration-dependent decreases in ATP were observed for sodium carbonate and 3-methylindole, with EC(50) values estimated as 2.57 and 0.91 mM, respectively. Acetic acid only decreased ATP significantly at the 100-mM concentration. In summary, this in vitro model has predicted the nasal toxicity of several compounds, including both direct-acting agents (sodium carbonate, acetic acid) and one requiring metabolic activation (3-methylindole). However, the lack of airflow-dependent dosimetry, results in some lack of discrimination between the different regions of the nasal cavity and may make this model overly sensitive.

Acetic Acid↗
PubMed2005

Complex mixture toxicity for single and multiple species: proposed methodologies.

Methods for the assessment of ecological risks associated with exposure to defined mixtures of toxicants are reviewed and formalized for single-species toxicity. Depending on the modes of action of toxicants in a mixture, these methods apply either the model for concentration additivity (CA) or the model for response additivity (RA). For complex mixtures, the present paper advocates the use of a new, two-step, mixed-model approach as a logical extension of model selection: Mixture toxicity for individual modes of action is evaluated with the CA model, and the toxicities of different modes of action are combined using the RA model. Using comparable mixture toxicity strategies in combination with the concept of species-sensitivity distributions, we develop a method to address and predict the risk for direct effects on the composition of species assemblages and biodiversity. The data needed for modeling can be obtained from existing databases, and lack of data can, in part, be addressed by the use of toxicity patterns in those databases. Both single- and multiple-species methods of mixture risk prediction are useful for risk management, because they allow ranking of polluted sites and affected species as well as identification of the most hazardous contaminants, at least in a comparative way. Validation of the proposed methods is feasible but currently limited because of a lack of appropriate data.

Animals↗
PubMed1982

[Neurotoxic substances as a tool to understand some mechanisms of peripheral neuropathies (author's transl)].

The study of toxic experimental models of neuropathies has been a decisive step to understand some cellular mechanisms of human neuropathies. The progressive development of toxic neuropathies allow to the possibility of isolating their initial mechanism. Dying back axonopathies are the commonest neuropathies as observed in clinical practice, and their experimental models had been extensively studied. Acrylamide and n-hexane intoxications have shown the following results : 1) The onset of the neuropathy is located at the most distal node of the longest and largest fibres. Sensory fibres are impaired before the motor ones. 2) Fast axoplasmic transport stops distally. 3) Impaired enzymes of the energetic cycle were observed distally. Proximal axonopathies as those resulting from IDPN intoxication are a possible model to clear up the cellular mechanisms of the lateral amyotrophic sclerosis. Human toxic neuronopathies and myelinopathies are uncommon. Such experimental models are described in relation to other human neuropathies.

Acrylamides↗
PubMed1997

Location of the toxic molecule abietic acid in model membranes by MAS-NMR.

Abietic acid, the major component of conifer oleoresin, is an environmental toxic molecule with potential hazard to animal and plant life. Being amphipatic, the study of its location and the interaction with membrane components is important to get insight into the mechanism of its toxic action. High resolution magic angle spinning natural abundance 13C nuclear magnetic resonance studies have been undertaken in order to assess its location in egg yolk phosphatidylcholine multilamellar vesicles model membranes. 13C spin-lattice relaxation times in the presence of Gd3+, a paramagnetic agent, of both the phospholipid and abietic acid molecules have been measured in order to obtain information on molecular distances (see J. Villalaín, Eur. J. Biochem. 241 (1996) 586-593). The molecule of abietic acid is placed in the upper part of the palisade structure of the membrane, its carboxyl group is in close proximity to the phospholipid ester groups and it does not extend beyond the C4/C7 carbons of the phospholipid molecule.

Abietanes↗
PubMed1994

Modeling fetal death and malformation in developmental toxicity studies.

We review approaches to dose-response modeling and risk assessment for binary data from developmental toxicity studies. In particular, we focus on jointly modeling fetal death and malformation and use a continuation ratio formulation of the multinomial distribution to provide a model for risk. Generalized estimating equations are used to account for clustering of animals within litters. The fitted model is then used to calculate doses corresponding to a specified level of excess risk. Two methods of arriving at a lower confidence limit or Benchmark dose are illustrated and compared. We also discuss models based on single binary end points and compare our approach to a binary analysis of whether or not the animal was 'affected' (either dead or malformed). The models are illustrated using data from four developmental toxicity studies in EG, DEHP, TGDM, and DYME conducted through the National Toxicology Program.

Abnormalities, Drug-Induced↗
PubMed2000

Post-injury ex vivo model to investigate effects and toxicity of pharmacological treatment in rings of rabbit aortic vessels.

Animal experiments are widely accepted in arteriosclerosis research. The aim of the present study was to establish an organ culture model (rings of rabbit aortic vessels) to investigate inhibitory estrogen effects on post injury neointima formation in the vessel wall and to examine whether these effects are cytotoxic. Estrogens are used for secondary prevention of atherosclerosis in postmenopausal women (estrogen replacement therapy/ERT). Phytoestrogens as well as the ovarian 17 beta-estradiol have been demonstrated to inhibit proliferation and migration of vascular smooth muscle cells which are key events in atherogenesis and restenosis after coronary angioplasty. In situ endothelial denudation of the thoracic and abdominal aorta was performed in female rabbits by a 3F Fogarty catheter. Segments of 5 mm were randomized in groups of n = 12 and held in culture. 17 beta-estradiol, Genistein and Daidzein were applied in concentrations of 20 microM, 30 microM, and 40 microM. Groups without estrogen treatment served as controls. The segments were investigated after 21 days. Afterwards, 3 further groups (n = 12) were held with the lowest concentrations of 17 beta-estradiol or the two phytoestrogens having been evaluated to inhibit the neointima formation significantly. After 21 days of treatment these sections were held in medium only for another 7 days to proof whether these segments were still able to proliferate. A denuded control group was held in medium only over 28 days. Compared to controls, 30 microM 17 beta-estradiol, 20 microM Genistein, and 40 microM Daidzein inhibited neointima formation significantly over 21 days. After another 7 days of cultivation in medium only the amount of neointima formation was comparable to that of non-estrogen-treated controls after 21 days. We therefore suggest that the demonstrated inhibitory effect is not explained by toxicity. In conclusion, by the use of this organ culture model it was possible to demonstrate non-toxic post injury effects of different estrogens in the vasculature. Because 24 aortic segments could be taken from one aortic vessel, the number of animals that would have been necessary for an experiment (8 to 10 per group for statistical reasons) could be markedly reduced. The results are of clinical interest because phytoestrogens and 17 beta-estradiol may offer therapeutic options for patients after coronary angioplasty regarding the process of restenosis. Because phytoestrogens do not affect the reproductive system they can also be used in men.

Animals↗
PubMed2002

Impact of preimmunization on adenoviral vector expression and toxicity in a subcutaneous mouse cancer model.

Immune responses against adenoviral vectors may influence the toxicity and therapeutic effectiveness of adenovirus-mediated gene transfer and may be a limiting factor in adenovirus-mediated gene therapy. The purpose of this study was to determine the effects of preimmunization on intratumoral adenoviral transduction and systemic spread. The hypothesis was that increased doses of adenoviral vectors could overcome local neutralization without added systemic toxicity. The level and duration of gene expression were assessed as a function of time and dose after intratumoral delivery of adenoviral vector (AdV) encoding the luciferase reporter gene (AdV-luc) in a subcutaneous mouse mammary tumor model. Preimmunization resulted in significantly decreased gene expression in tumor and normal tissues (P < 0.01). The decrease was significantly greater in liver than in tumor. Increased AdV doses could be used to overcome the intratumoral inhibition without a concomitant increase in liver transduction. However, preimmunized animals showed greater toxicity than nai;ve animals (P < 0.001). The preimmunized group developed histologic evidence of grade 2-3 hepatic toxicity and increases in the average values of hepatic enzymes. In addition, there was a significant increase in mortality (P < 0.01) in the preimmunized group (12 of 20 animals) compared with the naive group (3 of 20 animals). These findings suggest that although preimmunity can inhibit systemic expression from adenoviral vectors, at high vector doses it may potentiate hepatotoxicity.

Animals↗
PubMed2004

Patient characteristics compete with dose as predictors of acute treatment toxicity in early phase clinical trials.

PURPOSE: The purpose of this study was to identify patient characteristics that may be risk factors or markers of susceptibility to adverse treatment effects in cancer Phase I and II clinical trials. PATIENTS AND METHODS: A total of 459 patients enrolled in 23 therapeutic Phase I and II studies at the Fox Chase Cancer Center were included in the analysis. Patient-specific characteristics, medical and treatment history, doses of experimental agents, and graded toxicities were extracted from case report forms. We developed a novel summary measure, the toxicity index (TI), to better discriminate patients on the basis of their overall toxicity experiences. Mixed model ANOVA was used to model TI on the basis of data from all trials using a specific agent. Generalized estimating equations in the context of binary logistic regression were used to model dose-limiting toxicity. RESULTS: Seventeen pretreatment factors, including performance status, alkaline phosphatase, total bilirubin, serum creatinine, and tobacco use, emerged as significant predictors of toxicity as defined by dose-limiting toxicity or TI. Unexpectedly, dose was not always a predictor of toxicity. Even for values within the normal range, the TI identified serum bilirubin and alkaline phosphatase as predictors of toxicity after treatment with docetaxel and alkaline phosphatase as a predictor for toxicity after treatment with irinotecan. CONCLUSIONS: Independent of dose, certain pretreatment characteristics, including measures of organ function that are in the normal range, were found to be predictors of treatment toxicity. Because of its sensitivity to differences in overall toxicity, the TI should prove to be a useful tool for identifying predictors of chemotherapy-related toxicity.

Adult↗
PubMedDate not supplied

'Oxygen toxicity' induced by isoproterenol oxidation on living cells. An in vitro prokaryotic model.

Oxygen radical damage is a relevant problem in gerontological research. It has been implicated both in the aging process itself and in aging-related pathologies. Oxygen radicals from catecholamines seem to play an important role in central nervous system and cardiovascular system disorders during aging. Prokaryotic experimental systems have been shown to provide a simple and short term in vitro model for 'oxygen toxicity' from catecholamine oxidation which might be useful also in age-related research. In this paper we show that the synthetic sympathomimetic catecholamine, isoproterenol, oxidizes when added to bacteriological media and that this oxidation process causes bacterial growth inhibition. Both isoproterenol oxidation and the growth-inhibitory activity can be prevented by the addition of antioxidants. The addition of exogenous catalase (CAT), while unable to prevent isoproterenol oxidation, totally suppressed the bacterial growth inhibition; the addition of exogenous superoxide dismutase partially antagonized isoproterenol oxidation and suppressed bacterial growth inhibition although less efficiently than CAT. The model described suggests that besides 'oxygen toxicity' by endogenous natural catecholamines, iatrogenic tissue injury caused by the oxidation intermediates from this class of pharmacological compounds must also be considered.

Journal Article↗
PubMed2005

Variation in, and causes of, toxicity of cigarette butts to a cladoceran and microtox.

Cigarette butts are the most numerically frequent form of litter in the world. In Australia alone, 24-32 billion cigarette butts are littered annually. Despite this littering, few studies have been undertaken to explore the toxicity of cigarette butts in aquatic ecosystems. The acute toxicity of 19 filtered cigarette types to Ceriodaphnia cf. dubia (48-hr EC50 (immobilization)) and Vibrio fischeri (30-min EC50 (bioluminescence)) was determined using leachates from artificially smoked cigarette butts. There was a 2.9- and 8-fold difference in toxicity between the least and most toxic cigarette butts to C. cf. dubia and V. fischeri, respectively. Overall, C. cf. dubia was more inherently sensitive than V. fischeri by a factor of approximately 15.4, and the interspecies relationship between C. cf. dubia and V. fischeri was poor (R(2) = 0.07). This poor relationship indicates that toxicity data for cigarette butts for one species could not predict or model the toxicity of cigarette butts to the other species. However, the order of the toxicity of leachates can be predicted. It was determined that organic compounds caused the majority of toxicity in the cigarette butt leachates. Of the 14 organic compounds identified, nicotine and ethylphenol were suspected to be the main causative toxicants. There was a strong relationship between toxicity and tar content and between toxicity and nicotine content for two of the three brands of cigarettes (R(2 )> 0.70) for C. cf. dubia and one brand for V. fischeri. However, when the cigarettes were pooled, the relationship was weak (R(2) < 0.40) for both test species. Brand affected the toxicity to both species but more so for V. fischeri.

Aliivibrio fischeri↗