Journal articles: 'H+ toxicity'

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Dodd, Darol E., Gary M. Hoffman, and Colin J. Hardy. "Perfluoro-n-Butyl Iodide: Acute Toxicity, Subchronic Toxicity and Genotoxicity Evaluations." International Journal of Toxicology 23, no. 4 (July 2004): 249–58. http://dx.doi.org/10.1080/10915810490502050.

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Perfluoro-n-butyl iodide (PFBI) is a promising alternative to chlorofluorocarbon solvents used in aircraft ground maintenance operations and other military and commercial operations, because it cleans well, has zero ozone depletion potential, and has extremely low global warming properties. Toxicity tests were performed with PFBI to determine and evaluate its health hazard. Using standard testing guidelines (e.g., Organization for Economic Cooperation and Development [OECD]), tests included acute (4-h) and 4-week (6 h/day, 5 days/week) inhalation (nose-only) toxicity studies in rats, acute (10-min) inhalation cardiac sensitization study in dogs, in vitro chromosomal aberrations experiments in human lymphocytes, and in vitro mutagenic experiments in Salmonella typhimurium and Escherichia coli. There were no mortalities in rats ( n = 10) exposed for 4 h to 10,000 ppm PFBI, but all rats ( n = 10) died within 2 h when exposed to 20,000 ppm PFBI. The 4-h LC50 (95% confidence limits) was 14,000 ppm (13,000 ppm to 16,000 ppm). Signs (nasal discharge and labored breathing) observed in the rats exposed to 10,000 ppm returned to normal within 48 h. PFBI has the potential to cause cardiac sensitization in epinephrine-challenged dogs at 6200 ppm. A concentration of 3900 ppm was a no-observed-adverse-effect level (NOAEL) in the cardiac sensitization study. In the 4-week inhalation study (5 rats/sex/group), respiratory mucosal hypertrophy/hyperplasia was observed in rats of the 10,000-ppm group. A NOAEL of 1000 ppm was selected for the 4-week study on the basis that the mild increase in T4 observed at 1000 ppm was considered adaptive, not adverse, because of the absence of frank effects in the thyroid. In the in vitro studies, PFBI showed no evidence of either mutagenic or clastogenic activity. The toxicity profile of PFBI was compared to trifluoroiodomethane. In conclusion, the results of these studies indicate a low order of general toxicity and an absence of genotoxicity following PFBI exposure.

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Aidar, Elizabeth, Teresa C. S. Sigaud-Kutner, Márcia C. Bicega, Katya P. Schinke, Sania M. F. Gianesella, and Elisabete S. Braga. "Evaluation of produced water toxicity from an oil maritime terminal through Skeletonema costatum toxicity tests." Revista Brasileira de Oceanografia 47, no. 2 (1999): 137–44. http://dx.doi.org/10.1590/s1413-77391999000200003.

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The liquid effluent from an oil maritime terminal, with produced water as the main component, had its toxicity evaluated through toxicity tests with the diatom Skeletonema costatum. Two previously treated effluent samples (effluents A and B), were provided by PETROBRAS for the experiments. Both samples presented high salinity (67‰ for effluent A and 62‰ for effluent B) and low pH values (6.2), whereas total sulphide, phenol and nutrient content, dissolved/dispersed petroleum hydrocarbon concentration, BOD and COD values were quite different from each other. During the toxicity experiment, three replicate flasks with samples for each treatment were exposed to a light radiation of 266µE m² S-1 and maintained under a 10 h/14 h lightldark cycle, at a temperature of 24 :t 2ºC. The EC50 values could not be accurately estimated for effluent A: 60 h and 132 h after starting the experiment they were below 3% and between 3-6% effluent concentration, respectively. Synergistic effects between effluent toxicity and salinity on the growth of S. costatum were detected. The effluent B showed higher toxicity: the EC5O values were 0.17% and 0.40% of effluent concentrations, after 48 h and 96 h, respectively. These results evidenced the deleterious effects of residual organic compounds contained in the aqueous effluents from the oil terminal under the present pretreatment on S. costatum. In the light of the present data, the direct disposal ofthese effluents into São Sebastião Channel waters might be very hazardous to its indigenous biota.

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Cav, Spencer B., Stuart Berr, and Daniel C. Han. "Cyclosporin Toxicity in the Dog Kidney h Vido." Investigative Radiology 26, no. 12 (December 1991): 1141. http://dx.doi.org/10.1097/00004424-199112000-00103.

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Shukla, Madhulekha, and Sunita Arya. "CADMIUM TOXICITY INDUCED MORPHOLOGICAL ALTERATION IN INDIGENOUS FISH Heteropneustes fossilis (Bloch.)." Green Chemistry & Technology Letters 3, no. 1 (October 7, 2017): 21–25. http://dx.doi.org/10.18510/gctl.2017.315.

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The aim of present study was to determine the toxicity (LC50) of cadmium chloride in freshwater catfish Heteropneustes fossilis. Acute toxicity of cadmium on the indigenous fish H., fossilis was designed in the fish aquarium in laboratory at room temperature in Department of Zoology, DGPG College at Kanpur.Treated fish H., fossilis induced morphological alteration against cadmium chloride toxicity. H. fossilis showed morphological alteration such as increased opercula movement, abnormal swimming, and loss of buoyancy and fading of their body colour. Control fishes were also continuously monitored and compared with the changes caused by cadmium concentration. Heteropneustes fossilis exposed different concentration of cadmium chloride toxicity i.e. 0 ppm for 24 h, 10 ppm for 48h, 15ppm for 72h and 20 ppm for 96 h. From this present study it seems that the indigenous fish, H. fossilis is more susceptible to cadmium toxicity.

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Raipulis, Jēkabs, Malda Toma, and Maija Balode. "Toxicity and Genotoxicity Testing of Roundup." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 63, no. 1-2 (January 1, 2009): 29–32. http://dx.doi.org/10.2478/v10046-009-0009-6.

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Toxicity and Genotoxicity Testing of Roundup Glyphosate, in the commercial formulation named Roundup, is a broad spectrum herbicide that is one of the most frequently applied pesticides in the world. However, there has been little evidence of Roundup toxicity or genotoxicity. Genotoxicity of glyphosate was carried out using the Escherichia coli SOS chromotest. The glyphosate-induced dose response in the SOS chromotest suggests that glyphosate possesses genotoxic properties. Glyphosate at a 0.2 g/l concentration in toxicity bioassay caused 50% mortality of Daphnia magna (LD50 after 24 h — 0.22 g/l; after 48 h — 0.19 g/l), but 0.25 — 0.5 g/l — 100% death of organisms (LD100 after 24 h — 0.5 g/l; after 48 h — 0.25 g/l). Our results (E. coli SOS chromotest and daphnia test system) together with recent animal studies and epidemiological reports suggest that glyphosate, especially, Roundup possesses both toxic and genotoxic properties.

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Mustafa, Mohamad G. "Biochemical basis of ozone toxicity." Free Radical Biology and Medicine 9, no. 3 (January 1990): 245–65. http://dx.doi.org/10.1016/0891-5849(90)90035-h.

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McCalla, Laura B., Bryn M. Phillips, Brian S. Anderson, Jennifer P. Voorhees, Katie Siegler, Katherine R. Faulkenberry, Maurice C. Goodman, Xin Deng, and Ron S. Tjeerdema. "Effectiveness of a Constructed Wetland with Carbon Filtration in Reducing Pesticides Associated with Agricultural Runoff." Archives of Environmental Contamination and Toxicology 82, no. 3 (January 5, 2022): 317–29. http://dx.doi.org/10.1007/s00244-021-00909-0.

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AbstractThe Salinas Valley in Monterey County, California, USA, is a highly productive agricultural region. Irrigation runoff containing pesticides at concentrations toxic to aquatic organisms poses a threat to aquatic ecosystems within local watersheds. This study monitored the effectiveness of a constructed wetland treatment system with a granulated activated carbon (GAC) filter installation at reducing pesticide concentrations and associated toxicity to Ceriodaphnia dubia, Hyalella azteca, and Chironomus dilutus. The wetland was supplied with water pumped from an impaired agricultural and urban drainage. Across five monitoring trials, the integrated system’s average pesticide concentration reduction was 52%. The wetland channel and GAC filtration components individually provided significant treatment, and within each, pesticide solubility had a significant effect on changes in pesticide concentrations. The integrated treatment system also reduced nitrate by 61%, phosphate by 73%, and turbidity by 90%. Input water was significantly toxic to C. dubia and H. azteca in the first trial. Toxicity to C. dubia persisted throughout the system, whereas toxicity to H. azteca was removed by the channel, but there was residual toxicity post-GAC. The final trial had significant input toxicity to H. azteca and C. dilutus. The channel reduced toxicity to H. azteca and removed toxicity to C. dilutus. GAC filtration reduced H. azteca toxicity to an insignificant level. There was no input toxicity in the other three trials. The results demonstrate that a wetland treatment system coupled with GAC filtration can reduce pesticide concentrations, nutrients, suspended particles, and aquatic toxicity associated with agricultural runoff.

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Diaz, Lina Maria Caceres, Claudia Campos, and Gideon Oron. "Toxicity Effects of Selected Heavy Metals on Lactuca sativa and Hydra viridissima used for Sustainable Crop Production." Environmental Management and Sustainable Development 7, no. 3 (July 30, 2018): 82. http://dx.doi.org/10.5296/emsd.v7i3.13446.

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This study examines the prospects for using Hydra viridissima toxicity test 96-h LC50, served as a model invertebrate, Lactuca sativa L. was applied for seeds toxicity test (120-h IC50) and a model plant for an acute toxicity assessment of heavy metals content in water. The heavy metals used to assess the acute toxicity of the water utilized for agricultural irrigation in arid regions includes cadmium (CdCl2.2H2O), chromium (K2Cr2O7), zinc (ZnSO4. 7H2O), and boron (H3BO3). A grading of the substances was conducted, and it was found that the toxicity levels for H. viridissima and L. sativa were, with the least harmful first: B < Cr < Zn < Cd and Zn < B < Cr < Cd, respectively. Results indicate that H. viridissima was a more sensitive indicator of toxicity for all of the evaluated substances. However, L. sativa could also be used successfully to rank toxicants in order of their potential hazards.

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Curtis, Lawrence R., Wayne K. Seim, Lisbeth K. Siddens, Debra A. Meager, Richard A. Carchman, Walter H. Carter, and Gary A. Chapman. "Role of Exposure Duration in Hydrogen Ion Toxicity to Brook (Salvelinus fontinalis) and Rainbow Trout (Salmo gairdneri)." Canadian Journal of Fisheries and Aquatic Sciences 46, no. 1 (January 1, 1989): 33–40. http://dx.doi.org/10.1139/f89-005.

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Acidification of streams and rivers associated with rainstorm or snowmelt events is often episodic as are many environmental introductions of toxic substances. We examined the toxicity of continuous or intermittent exposures to sulfuric acid (H+) to brook trout (Salvelinus fontinalis) embryos, alevins, and fry. Acute toxicity tests were conducted with juvenile rainbow trout (Salmo gairdneri). These studies permitted evaluation of key components of intermittent exposures (toxicant concentration, exposure duration, and recovery period) on mortality, reduced growth, and perturbed electrolyte balance. Lethality of H+ markedly changed with developmental stage of brook trout. Resistance of the chorion to H+ penetration probably protected embryonic fish, while hatching and onset of active swimming exacerbated H+ toxicity. Response surface methods demonstrated that between pH 4 and 7, time–concentration relationships for H+ toxicity were greatly influenced by exposure duration and peak concentration but little by length of recovery period. Daily pulses at pH 4 with duration as short 4.5 h produced marked mortality after 90 d. This did not occur after 4–60 d of testing. Whole-body Na+, K+, and Ca2+ concentrations of brook trout were negatively correlated with mean H+ concentrations after 90 d of exposure. Cation depletion appeared to be a more sensitive index of chronic, sublethal H+ toxicity than reduced growth.

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10

Reid, B. L., and G. W. Bennett. "Dietary Toxicity Trial, 1987." Insecticide and Acaricide Tests 14, no. 1 (January 1, 1989): 382. http://dx.doi.org/10.1093/iat/14.1.382a.

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Abstract Laboratory tests evaluated the toxicity of the dihaloalkyl arylsulfone biocide, A-9248 (diiodomethyl para-tolyl sulfone), when fed continuously to German cockroach nymphs from the second and fifth (last) nymphal stage until adulthood. The toxicants were formulated into diets prepared by finely grinding Wayne Rodent Blox into 5-g portions and reconstituting each with 6 ml of water and 3 ml of an acetone solution of technical A-9248. This was mixed thoroughly, pressed into plexiglass molds, and allowed to dry for 48 h within an evacuation hood, yielding pelletized diets (75-100 mg) of the desired concentration (% AI). Seven diet concentrations (10-0.156%; 0.5 times serial dilutions) were evaluated to achieve a clear representation of A-9248 activity. Groups of 10 unsexed, newly eclosed (<24 h) second- or fifth-stage nymphs were placed into 100- by 25-mm vented plastic Petri dishes supplied with test diet, water vial, and cardboard harborage. Each diet concentration was replicated 6 times, for a total of 60 nymphs/dilution rate.

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11

Ding, Guang Hui, Jing Zhang, Yi Hong Chen, Guo Yi Luo, and Chao Hong Mao. "Acute Toxicity Effect of PFOS on Zebrafish Embryo." Advanced Materials Research 356-360 (October 2011): 603–6. http://dx.doi.org/10.4028/www.scientific.net/amr.356-360.603.

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Perfluorooctane sulfonate (PFOS) has emerged as one of the most concerning contaminants in recent years. In the present study, the developmental toxicity of PFOS on zebrafish embryo was tested. The EC50based on the general morphology score are 78.13 and 76.53 mg/L for 96 h and 120 h, respectively. While the LC50values for 96 h and 120 h are 79.08 and 70.17 mg/L, respectively. It was found PFOS resulted in the decrease of heart rate of zebrafish embryo, while had some degree of stimulation at 40 mg/L PFOS.

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12

Vogel, Christoph. "Prostaglandin H Synthases and their Importance in Chemical Toxicity." Current Drug Metabolism 1, no. 4 (December 1, 2000): 391–404. http://dx.doi.org/10.2174/1389200003338884.

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13

Zhang, Quancheng, Zemin He, and Jungang Wang. "Acute Toxicity, Oxidative Stress, Toxicity Mechanism, and Degradation Dynamics of Trifluralin in Eisenia foetide (Annelida: Lumbricidae)." Journal of Entomological Science 58, no. 1 (January 1, 2023): 27–46. http://dx.doi.org/10.18474/jes22-06.

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Abstract Trifluralin is a preemergent herbicide that is applied to soil to control annual grasses and broadleaf weeds. It is widely used in cotton, Gossypium hirsutum L., production in China; however, the ecological safety of its continued use is a controversial issue. We studied the interaction of trifluralin and earthworms, Eisenia foetide Savigny (Annelida: Lumbricidae), to provide additional information for assessing the risk of trifluralin to ecological safety in soils. Contact toxicity assays established median lethal concentrations (LC50) of 726.298 µg/L at 24 h, 418.783 µg/L at 48 h, and 82.007 µg/L at 72 h of exposure to trifluralin. Within 24 to 48 h of exposure to trifluralin, antioxidant activity (e.g., superoxide dismutase, catalase, peroxidase) increased in vivo, but by 72 h of exposure the activity was inhibited and, at high concentrations of trifluralin, death occurred. Based on the activity of glutathione S-transferase (GST) and multifunction oxidase (MFO), it appears that GSTs may be involved in the detoxification of trifluralin in vivo, and that MFOs may be the key detoxification enzymes involved. Earthworm degradation of trifluralin shortened the half-life of trifluralin in soil by as much as 1.78 d. These results provide useful information on the toxicity mechanism of trifluralin in earthworms, the role of earthworms in trifluralin degradation, as well as the ecological safety of trifluralin.

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Gut, Josef, Urs Christen, and Jörg Huwyler. "Mechanisms of halothane toxicity: Novel insights." Pharmacology & Therapeutics 58, no. 2 (January 1993): 133–55. http://dx.doi.org/10.1016/0163-7258(93)90047-h.

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15

Verma, Y. "Acute toxicity assessment of textile dyes and textile and dye industrial effluents using Daphnia magna bioassay." Toxicology and Industrial Health 24, no. 7 (August 2008): 491–500. http://dx.doi.org/10.1177/0748233708095769.

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Aquatic toxicity of textile dyes and textile and dye industrial effluents were evaluated in an acute toxicity study using Daphnia magna as an aquatic experimental animal model. The 48-h EC50 value for the azo dyes, Remazol Parrot Green was 55.32 mg/L and for Remazol Golden Yellow was 46.84 mg/L. Whereas 48-h EC50 values for three dye industrial effluents (D1, D2, and D3) were 14.12%, 15.52%, and 29.69%, respectively. Similarly, EC50 value for three textile mill effluents (T1, T2, and T3) were >100%, 62.97%, and 63.04%, respectively. These results also showed linear relationship with high degree of confidence ( r2 = >0.84 to >0.99) between immobility and test concentrations. The ratio of 24 to 48-h EC50 remains to be in between 1.1 and 1.2. The general criteria of toxicity classification showed that both dyes were minor acutely toxic having 48-h EC50 in between 10 and 100 mg/L. Of the six textile and dye industrial effluents tested, one was not acutely toxic (48-h EC50 > 100%) and five were minor acutely toxic (48-h EC50 > 14.12–29.69%). The toxicity classification of effluent based on toxic unit (TU) showed that of the six effluents tested five were found toxic (TU = >1) and one was non-toxic (TU = <1). Thus, dye effluents showed highest toxicity and textile effluents lowest toxicity. The study also suggested that the assay with D. magna was an excellent method for evaluation of aquatic toxicity of dyes and dyes containing industrial effluents.

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Vyskocil, Adolf, Claude Viau, and Serge Lamy. "Peroxyacetyl nitrate: review of toxicity." Human & Experimental Toxicology 17, no. 4 (April 1998): 212–20. http://dx.doi.org/10.1177/096032719801700403.

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PAN is one of a class of common air pollutants formed by the action of sunlight on volatile organic compounds and nitrogen oxides. No toxicokinetic studies have been found in the available literature. The acute toxicity of PAN is less than that of ozone, similar to NO2 and higher than SO2. The LC50 in mice and rats were 718-743 mg/m3 (for 2 h) and 470 mg/m3 (for 4 h), respectively. Following acute exposure, severe lung lesions and, at the higher levels, damage to the epithelium of upper parts of the respiratory tract were found in animals. It seems that concentrations of 1.19-1.49 mg/m3 lie not far from the threshold required for pulmonary function effects in sensitive individuals. However, these PAN concentrations are well above the maximum ambient concentrations usually experienced within the USA and Canada (0.003-0.078 mg/m3). It appears unlikely that present ambient PAN concentrations would affect pulmonary functions responses to ambient ozone. In human, the lowest level causing eye irritations was 0.64 mg/m3 for 2 h. Concentrations of 0.99 and 4.95 mg/m3 were identi-fied as no-observed-effect level (NOEL) and no-observed-adverse-effect level (NOAEL) for pathological and histo-logical changes in the respiratory system (nasal passages) of rats during subchronic exposures to PAN, but were not considered to be relevant to derivation of a RfC for chronic inhalation exposure. PAN is a weak point mutagen or clastogen. The data are not sufficient to evaluate its carcinogenicity. No study was found which could be used for the derivation of a RfC for acute or chronic inhalation exposure to PAN.

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Abreo, K., J. Jangula, S. K. Jain, M. Sella, and J. Glass. "Aluminum uptake and toxicity in cultured mouse hepatocytes." Journal of the American Society of Nephrology 1, no. 12 (June 1991): 1299–304. http://dx.doi.org/10.1681/asn.v1121299.

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Hepatic aluminum (Al) accumulation in association with hepatobiliary dysfunction has been described in children receiving contaminated parenteral alimentation solutions and in aluminum-overloaded experimental animals. The mechanisms of hepatic Al uptake are not clearly understood, and it is not known whether Al is directly toxic to the hepatic cell or if toxicity occurs from the effect of Al on hepatic iron (Fe) metabolism. Al causes a microcytic hypochromic anemia and concomitant hepatic Al and Fe can accumulate in dialysis patients, suggesting that Al may alter Fe metabolism. Therefore, Al uptake and toxicity were studied in mouse hepatocytes in culture. Al accumulation, cell growth, media hepatic enzyme concentrations, and cell malonyldialdehyde concentrations, a marker of membrane lipid peroxidation, were measured in mouse hepatocytes grown in media containing either Al citrate, transferrin-Al (Tf-Al), or no additions over 96 h. Al uptake occurred only in cells grown in Tf-Al and Al citrate at 24 h and increased linearly achieving cellular concentrations at 96 h of 522 +/- 36 and 186 +/- 12 micrograms/L, respectively, compared with 31 +/- 3 micrograms/L (P less than 0.001) in control media. Inhibition of cell growth occurred at 48, 72, and 96 h (P less than 0.001), and media lactate dehydrogenase and aspartate aminotransferase concentrations increased starting at 48 and 72 h, respectively (P less than 0.001), only in media containing Tf-Al. Cell malonyldialdehyde levels were significantly higher in Tf-Al-loaded mouse hepatocytes compared with control cells at 96 h (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Richards, Laura, Stephanie Walsh, Carmen Shultz, and Marilyne Stuart. "ASSESSMENT OF THE EFFECT OF WATER QUALITY ON COPPER TOXICITY INHYALELLA AZTECA." AECL Nuclear Review 4, no. 1 (June 1, 2015): 83–90. http://dx.doi.org/10.12943/anr.2015.00040.

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The objective of this study was to test the hypothesis that when standard artificial media 5-salt culture water (SAM-5S) is used to test sediment toxicity of much lower ionic-strength aquatic ecosystems, the resulting toxicity estimates are lower than if the tests had been conducted in water of comparable ionic strength. Results showed that this concern was unfounded for testing of copper toxicity to Hyalella azteca (H. azteca) in Ottawa River water. Sediment testing is often conducted using a standard water that is prepared in the laboratory. However, this water may have an ionic strength that is different than local water bodies. It follows that laboratory results using the standard water may be unrepresentative. A study was undertaken to assess the copper tolerance of 2 strains of H. azteca in SAM-5S, diluted SAM-5S (similar in electrical conductivity to Ottawa River water), and Ottawa River water. Acute (96 h) copper toxicity tests were conducted with 9–16 day-old H. azteca. For a given water type, the 2 strains of H. azteca yielded comparable responses to copper. The highest copper tolerance was found in Ottawa River water (closely followed by SAM-5S), whereas the lowest copper tolerance was found in diluted SAM-5S. Our results suggest that sediment toxicity is not lowered by the higher ionic strength of SAM-5S and that sediment toxicity tests of Ottawa River sediments, conducted with SAM-5S, can be used to estimate the in situ toxicity of the sediments.

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Frontzek, Karl, Marco Bardelli, Assunta Senatore, Anna Henzi, Regina R. Reimann, Seden Bedir, Marika Marino, et al. "A conformational switch controlling the toxicity of the prion protein." Nature Structural & Molecular Biology 29, no. 8 (August 2022): 831–40. http://dx.doi.org/10.1038/s41594-022-00814-7.

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AbstractPrion infections cause conformational changes of the cellular prion protein (PrPC) and lead to progressive neurological impairment. Here we show that toxic, prion-mimetic ligands induce an intramolecular R208-H140 hydrogen bond (‘H-latch’), altering the flexibility of the α2–α3 and β2–α2 loops of PrPC. Expression of a PrP2Cys mutant mimicking the H-latch was constitutively toxic, whereas a PrPR207A mutant unable to form the H-latch conferred resistance to prion infection. High-affinity ligands that prevented H-latch induction repressed prion-related neurodegeneration in organotypic cerebellar cultures. We then selected phage-displayed ligands binding wild-type PrPC, but not PrP2Cys. These binders depopulated H-latched conformers and conferred protection against prion toxicity. Finally, brain-specific expression of an antibody rationally designed to prevent H-latch formation prolonged the life of prion-infected mice despite unhampered prion propagation, confirming that the H-latch is an important reporter of prion neurotoxicity.

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Ding, Guang Hui, Jing Zhang, Man Wang, Yi Hong Chen, Guo Yi Luo, and De Qi Xiong. "Evaluation and Prediction of Mixture Toxicity of PFOS and PFOA to Zebrafish (Danio rerio) Embryo." Advanced Materials Research 485 (February 2012): 297–300. http://dx.doi.org/10.4028/www.scientific.net/amr.485.297.

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Perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) have emerged as two concerning contaminants in recent years. However, there is limited information about their mixture toxicity to aquatic organisms. In the present study, the single and mixture toxicity of PFOA and PFOS to zebrafish (Danio rerio) embryo were tested, and the mixture toxicity was predicted by concentration addition (CA) and independent action (IA) models. It is found that PFOS and PFOA have synergistic effect at 96 hpf, while this kind of synergistic effect is not obvious at 72 hpf. CA and IA models both could predict the 72 h mixture toxicity, while underestimate the 96 h mixture toxicity.

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KENTHAO, Anan, Wanchat SIRISARN, and Pornpimol JEARRANAIPREPAME. "Acute Toxicity of Cypermethrin on Nile tilapia Fry." Walailak Journal of Science and Technology (WJST) 17, no. 7 (July 1, 2020): 708–18. http://dx.doi.org/10.48048/wjst.2020.3815.

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The present study aimed to evaluate the acute toxicity effect of cypermethrin contaminated aquatic ecosystems by using a 30 days post-hatching fry of Nile tilapia as a test model. The control and six test experiments, each comprising 10 animals, were repeated three times and evaluated with the static test method. The lethal concentrations at 50 % (LC50) and 70 % (LC70) for 96 h were determined using the probit analysis. Behavioural and histological changes were observed in fish exposed with cypermethrin at both 96 h LC50 and 96 h LC70. The values of 96 h LC50 and 96 h LC70 were estimated at 32.496 and 40.311 ppb, respectively. The affected fish exhibited the loss of equilibrium with erratic and darting swimming movements, hyperactivity, secretion of mucous and increasing rate of opercula activity. Severity of histopathological lesions were related to concentration levels and exposure times. The histological changes of gill tissues included the swelling of epithelial cells and the fusion of secondary lamella. An enlargement of sinusoids, pyknotic nuclei, vacuole formation and degeneration in hepatic parenchyma were observed in liver. The degeneration of glomerulus combining with oedema of renal tubule was also noticed in kidney. No alter lesion was seen on skin tissue. The results in the present study suggest that low levels of cypermethrin in the aquatic environment may alter adverse effect on growth and development in Nile tilapia.

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Silva, Amélia M., Carlos Martins-Gomes, Tânia L. Silva, Tiago E. Coutinho, Eliana B. Souto, and Tatiana Andreani. "In Vitro Assessment of Pesticides Toxicity and Data Correlation with Pesticides Physicochemical Properties for Prediction of Toxicity in Gastrointestinal and Skin Contact Exposure." Toxics 10, no. 7 (July 8, 2022): 378. http://dx.doi.org/10.3390/toxics10070378.

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In this work, three pesticides of different physicochemical properties, namely, glyphosate (herbicide), imidacloprid (insecticide) and imazalil (fungicide), were selected to assess their cytotoxicity against distinct cell models (Caco-2, HepG2, A431, HaCaT, SK-MEL-5 and RAW 264.7 cells) to mimic gastrointestinal and skin exposure with potential systemic effect. Cells were subjected to different concentrations of selected pesticides for 24 h or 48 h. Cell viability was assessed by Alamar Blue assay, morphological changes by bright-field microscopy and the IC50 values were calculated. Cytotoxic profiles were analysed using the physico-chemical parameters of the pesticides, namely: molecular weight, water solubility, the partition coefficient in the n-octanol/water (Log Pow) system, the topological polar surface area (TPSA), and number of hydrogen-bonds (donor/acceptor) and rotatable bonds. Results showed that glyphosate did not reduce cell viability (up to 1 mM), imidacloprid induced moderate toxicity (IC50 > 1 mM for Caco-2 cells while IC50 = 305.9 ± 22.4 μM for RAW 264.7 cells) and imazalil was highly cytotoxic (IC50 > 253.5 ± 3.37 for Caco-2 cells while IC50 = 31.3 ± 2.7 μM for RAW 264.7 cells) after 24 h exposure. Toxicity was time-dependent as IC50 values at 48 h exposure were lower, and decrease in cell viability was accompanied by changes in cell morphology. Pesticides toxicity was found to be directly proportional with their Log Pow, indicating that the affinity to a lipophilic environment such as the cell membranes governs their toxicity. Toxicity is inverse to pesticides TPSA, but lower TPSA favours membrane permeation. The lower toxicity against Caco-2 cells was attributed to the physiology and metabolism of cell barriers equipped with various ABC transporters. In conclusion, physicochemical factors such as Log Pow, TPSA and H-bond are likely to be directly correlated with pesticide-induced toxicity, thus being key factors to potentially predict the toxicity of other compounds.

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Tognella, Sergio. "Pharmacological interventions to reduce platinum-induced toxicity." Cancer Treatment Reviews 17, no. 2-3 (September 1990): 139–42. http://dx.doi.org/10.1016/0305-7372(90)90038-h.

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Frankenhuyzen, Kees van, and Glen H. Geen. "Effects of low pH and nickel on growth and survival of the shredding caddisfly Clistoronia magnifica (Limnephilidae)." Canadian Journal of Zoology 65, no. 7 (July 1, 1987): 1729–32. http://dx.doi.org/10.1139/z87-267.

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In laboratory experiments with larvae of the shredding caddisfly Clistoronia magnifica, toxicity of nickel chloride hexahydrate was highly pH dependent. Larvae were exposed from first instar until pupation to three nickel concentrations (55, 215, 700 μg Ni2+/L) in soft water adjusted to pH 4.1, 5.5, and 6.2. Nickel reduced the survival of larvae and pupae at all pH levels but toxicity decreased with increasing H+ concentration. In addition, Ni at 215 μg/L temporarily ameliorated H+ toxicity to early instar larvae at pH 4.1. Reduced toxicity with decreasing pH fits the hypothesis that free metal ions compete with H+ for the same binding–uptake sites. Available data suggest that this phenomenon is not restricted to a particular metal or organism but that it applies to pH–metal interactions in general.

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INABA, Kei, Teruo KURODA, Toshi SHIMAMOTO, Takashi KAYAHARA, Masaaki TSUDA, and Tomofusa TSUCHIYA. "Lithium Toxicity and Na+(Li+)/H+ Antiporter in Escherichia coli." Biological & Pharmaceutical Bulletin 17, no. 3 (1994): 395–98. http://dx.doi.org/10.1248/bpb.17.395.

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ANDERSSON, O. "Toxicity of silica-containing calcium phosphate glasses Örjan H. Andersson." Biomaterials 14, no. 4 (1993): 317. http://dx.doi.org/10.1016/0142-9612(93)90125-l.

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Chandrama Singh, Shashi, Muskan Choudhary, Atul Mourya, Dharmendra Kumar Khatri, Pankaj Kumar Singh, Jitender Madan, and Harshpal Singh. "Acute and Subacute Toxicity Assessment of Andrographolide-2-hydroxypropyl-β-cyclodextrin Complex via Oral and Inhalation Route of Administration in Sprague-Dawley Rats." Scientific World Journal 2022 (March 28, 2022): 1–9. http://dx.doi.org/10.1155/2022/6224107.

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Objective. Acute and subacute toxicity analysis of AND-2-HyP-β-CYD complex was conducted in Sprague-Dawley (SD) rats following oral and inhalation routes of administration. Methods and Results. Single dose acute toxicity was carried out at 2000 mg/kg of AND-2-HyP-β-CYD complex, while the doses of 200, 400, and 666 mg/kg were administered, over a period of 28 days under repeated dose oral toxicity study. Hence, LD50 (lethal dose) was found to be >2000 mg/kg in addition to NOAEL (no observed adverse effect level) of 666 mg/kg. Correspondingly, single dose acute inhalation toxicity of AND-2-HyP-β-CYD complex was carried out at 5 mg/L/4 h/day and subacute inhalation toxicity at 0.5, 1, and 1.66 mg/L/4 h/day over a period of 28 days. The NOAEL and LOAEL (lowest observed adverse effect level) were estimated to be 0.5 mg/L/4 h/day and 1 mg/L/4 h/day, respectively. Conclusion. The findings of the present study would further be useful in assessing and utilizing the medicinal and therapeutic benefits of AND-2-HyP-β-CYD complex.

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Deneke, S. M., B. A. Lynch, and B. L. Fanburg. "Transient depletion of lung glutathione by diethylmaleate enhances oxygen toxicity." Journal of Applied Physiology 58, no. 2 (February 1, 1985): 571–74. http://dx.doi.org/10.1152/jappl.1985.58.2.571.

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Diethylmaleate (DEM) decreases glutathione (GSH) levels in various organs by enzymatic conjugation with reduced GSH catalyzed by GSH transferase. We have examined levels of GSH, glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PD) in lungs of 200–250-g rats after intraperitoneal injection of 0.5 or 1 g DEM/kg body wt. The GSH levels are severely depressed at 2 and 4 h but have essentially recovered by 12 and 24 h after either dose of DEM. The GR and G6PD activities in the 1 g/kg group are depressed at 4 h to a lesser extent than the GSH levels and also return to normal by 12 and 24 h. These enzymes are not affected in the 0.5 g/kg group. To determine whether these transient decreases in GSH and related enzymes affected O2 tolerance, we exposed rats injected with DEM to greater than 98% O2 and found that halftime (t1/2) for survival was decreased in rats receiving both 0.5 and 1 g DEM/kg body wt when compared with untreated or saline-injected controls (t1/2 control, 74 h; 0.5 g DEM, 59 h; 1 g DEM, 53 h). No deaths occurred in air controls at 1 mg/kg DEM for up to 5 days. DEM, in itself, caused no morphological alteration of the lung. Thus a decrease in lung GSH and related enzymes, occurring by 4 h and reversed by 12 h, has a significant effect on the subsequent progression of lung pathology and indicates that early biochemical events occurring in lungs exposed to hyperoxia may be very important in determining the degree of longer-term damage to rat lungs.

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29

Divya, Kajaria, Tripathi J. S, Tiwari S. K., and Pandey B. L. "An Evaluation of Acute Toxicity and Subchronic Toxicity of Hydroethanolic Extract of “Shirishadi”- A Polyherbal Ayurvedic Compound in Rodents." Biosciences, Biotechnology Research Asia 14, no. 2 (June 25, 2017): 567–76. http://dx.doi.org/10.13005/bbra/2480.

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ABSTRACT: This study was aimed at evaluating the safety profile, acute and subchronic toxicity of Shirishadi polyherbal ayurvedic compound in rodents, commonly used in the treatment of Bronchial Asthma. Acute toxicity was evaluated in wister albino rats by administering orally graded doses of extract of Albezzia lebbeck, Cyperus rotandus and Solanum xanthocarpum (Shirishadi Compound) in the dose of 2000, 5000 mg/kg, 10, and 20 g/kg body weight of animal and observed continuously for first 4 h and hourly for next 12 h, then 8 hourly for next 56 h (72 h, acute toxicity study). The study had been strictly followed the OECD guidance. Adult Wister albino rats were divided into 3 groups with 5 animals in each group and a control group, fed with doses of 5, 100 mg and 150 mg/ml once in a day for 30 days. Effect of drug was evaluated on hematological parameter after every 7 days and histological study was done after sacrificing the animals on 31st day. The median acute toxicity value (LD50) of the extract was found to be infinite and drug was found to be totally non toxic as after ingestion of 20 g no animal found to be dead. Hematological profile shows no abnormal elevation in level of Serum-Bilirubin, GOT, GPT, urea and creatinine. There was no any evidence of toxicity in histopathological studies.

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Beckett, W. S., and N. D. Wong. "Effect of normobaric hyperoxia on airways of normal subjects." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1683–87. http://dx.doi.org/10.1152/jappl.1988.64.4.1683.

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Airway responsiveness to inhaled cholinergic agonist during the early stage of pulmonary O2 toxicity was examined to determine whether normobaric hyperoxia alters airway function. Eight healthy nonsmoking males with moderate base-line methacholine responsiveness breathed normobaric O2 (greater than or equal to 95%) over 12 h and on another occasion breathed air in an identical protocol. Vital capacity, expiratory flow, airway responsiveness to methacholine, and respiratory symptoms were measured at 0, 4, 8, and 12 h while subjects breathed O2 and 12 h afterwards. After 12 h, forced vital capacity was significantly decreased with O2 breathing but not with air breathing. At 4, 8, or 12 h of exposure and 12 h after exposure, there was no difference in methacholine sensitivity or reactivity between O2 and air-exposure trials. The earliest manifestations of pulmonary normobaric O2 toxicity in normal adults include diminished vital capacity and the onset of respiratory symptoms, but early O2 toxicity does not produce altered responsiveness to inhaled methacholine.

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Spielberg, Stephen P. "Acetaminophen toxicity in lymphocytes heterozygous for glutathione synthetase deficiency." Canadian Journal of Physiology and Pharmacology 63, no. 5 (May 1, 1985): 468–71. http://dx.doi.org/10.1139/y85-081.

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We have studied the effects of acetaminophen metabolites generated by a murine hepatic microsomal system on lymphocytes from two subjects heterozygous for glutathione synthetase deficiency. Heterozygous cells exhibited greater dose-related toxicity than controls. Following a 2-h incubation with acetaminophen and the microsomal system, cells were washed and incubated for 16 h in the presence or absence of N-acetylcysteine, the standard antidote for acetaminophen toxicity. In control cells, glutathione content was replenished to nearly base-line values and toxicity was prevented. N-Acetylcysteine thus prevented toxicity even after covalent binding of acetaminophen metabolites had occurred. Heterozygous cells failed to use N-acetylcysteine as efficiently to resynthesize glutathione, and the cells were not protected from acetaminophen toxicity. Heterozygotes may be at increased risk of toxicity from drugs whose metabolites are detoxified by glutathione conjugation.

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Doe, K. G., W. R. Ernst, W. R. Parker, G. R. J. Julien, and P. A. Hennigar. "Influence of pH on the Acute Lethality of Fenitrothion, 2,4-D, and Aminocarb and Some pH-Altered Sublethal Effects of Aminocarb on Rainbow Trout (Salmo gairdneri)." Canadian Journal of Fisheries and Aquatic Sciences 45, no. 2 (February 1, 1988): 287–93. http://dx.doi.org/10.1139/f88-034.

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Three pesticides, fenitrothion, 2,4-D, and aminocarb, were tested in static 96-h acute lethal toxicity tests using fingerling rainbow trout (Salmo gairdneri) at pH 4.6, 5.6, 6.9, and 8.5. The toxicity of aminocarb, a base, increased significantly with increasing pH. Conversely, the toxicity of the acidic pesticide 2,4-D increased with decreasing pH. The toxicity of the neutral pesticide fenitrothion did not change significantly with changing pH. Subsequent tests were performed on trout fingerlings with aminocarb to determine the effect of two exposure pH's on brain acetylcholinesterase activity and whole-body aminocarb residue. Brain acetylcholinesterase was found to be inversely proportional to whole-body aminocarb content of fish. In fish exposed at pH 4.6, brain acetylcholinesterase was maximally depressed at 6 h, after which it recovered to within the control range. Whole-body aminocarb concentrations rose to a maximum within 6 h and subsequently declined to low levels. In fish exposed at pH 8.2, brain acetylcholinesterase dropped below the control range by 1 h and remained low until all fish died by 72 h. A maximum whole-body aminocarb concentration was reached within 1 h and remained elevated until the fish died. Several explanations for the observed results are presented.

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Hill, Walter R., Angela T. Bednarek, and I. Lauren Larsen. "Cadmium sorption and toxicity in autotrophic biofilms." Canadian Journal of Fisheries and Aquatic Sciences 57, no. 3 (March 1, 2000): 530–37. http://dx.doi.org/10.1139/f99-286.

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Autotrophic biofilms (periphyton) accumulate substantial quantities of metals from contaminated water. In this study, we measured the time course of biofilm cadmium sorption, examined the effects of current, biomass, and light on short-term cadmium sorption by biofilms, and tested the toxicity of cadmium to biofilm photosynthesis. The time course of cadmium sorption appeared to be a linear function of time over the 48-h measurement period. Biofilms in current [Formula: see text]2 cm·s-1 sorbed three to five times more cadmium than biofilms in still water. Cadmium sorbed after 4 h was 75% greater in high-biomass biofilm (2.5 mg dry mass·cm-2) than in low-biomass biofilm (0.5 mg dry mass·cm-2), but only in moving water. Light enhanced the sorption of cadmium 40% in one biofilm type. Cadmium toxicity to photo synthesis was evident after 24 h in thin biofilms exposed to initial cadmium concentrations [Formula: see text]10 μg·L-1; photosynthesis by thicker biofilms was not significantly impaired even at the highest concentration (100 μg·L-1). Variations in current, biofilm biomass, and light are likely to influence the movement of metals in flowing systems.

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34

France, Robert L., and Pamela M. Stokes. "Influence of manganese, calcium, and aluminum on hydrogen ion toxicity to the amphipod Hyalella azteca." Canadian Journal of Zoology 65, no. 12 (December 1, 1987): 3071–78. http://dx.doi.org/10.1139/z87-466.

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Experiments were undertaken to examine the influence of Mn and Ca on H+ and combined H+/Al toxicity to the amphipod Hyalella azteca in synthetic inorganic media. Aluminum concentrations of 0.25 and 0.40 mg∙L−1 at pH 4.8 and 0.40 mg∙L−1 at pH 4.3 significantly increased the rate of mortality compared with reference Al concentrations of 0.05 mg∙L−1 at these pH values. Concentrations of Al as high as 0.70 mg∙L−1 did not ameliorate H+ toxicity at pH 4.0. Toxicity was always dominated by the H+ effect. Variation in neither aqueous Ca concentration from 0.5 to 4.0 mg∙L−1 nor Mn from 0.10 to 0.40 mg∙L−1 had any significant effect on the survivorship of H. azteca exposed to lethal treatments of H+ and Al (pH 4.0–5.3; [Al] = 0.25–0.70 mg∙L−1). We predict that mortality of this amphipod from springmelt pulses will be determined primarily by [H+], and secondarily by [Al] (but only in the pH range 4.3–5.3), and will occur independently of any accompanying changes in [Ca] or [Mn].

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35

Baccalini, Alessio, Stefania Vergura, Pravas Dolui, Giuseppe Zanoni, and Debabrata Maiti. "Recent advances in cobalt-catalysed C–H functionalizations." Organic & Biomolecular Chemistry 17, no. 48 (2019): 10119–41. http://dx.doi.org/10.1039/c9ob01994d.

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Ready availability, low cost and low toxicity of cobalt salts have redirected the attention of researchers away from noble metals, such as Pd, Rh, and Ir, towards Co in the field of C–H functionalisation.

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36

Cittanova, Marie-Laure, Brigitte Lelongt, Marie-Christine Verpont, Monique Geniteau-Legendre, Fayez Wahbe, Dominique Prie, Pierre Coriat, and Pierre M. Ronco. "Fluoride Ion Toxicity in Human Kidney Collecting Duct Cells." Anesthesiology 84, no. 2 (February 1, 1996): 428–35. http://dx.doi.org/10.1097/00000542-199602000-00022.

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Background Several halogenated anesthetics induce a urinary concentrating defect, partly related to fluoride ion toxicity in collecting duct cells. The aim of this study was to investigate the effects of fluoride ion in human kidney cells. Methods Immortalized human collecting duct cells were used. In a first set of experiments, the toxicity threshold concentration was determined by exposing cell cultures for 24 h to increasing concentrations of fluoride ion in the medium: 0, 1, 5, and 10 mM. The second set of experiments was a time- effect study in which cells were exposed to 5 mM fluoride for 2, 6, and 24 h. Assessment of toxicity was based on several endpoints: cell number, protein content, (3)H-leucine incorporation in newly synthesized proteins, extracellularly released lactate dehydrogenase, Na-K-ATPase pump activity, and electron microscope studies. Results After 24 h of exposure, fluoride ion decreased cell number (-23%, P<0.05), total protein content (-30%, P<0.05) and increased lactate dehydrogenase release (+236%, P<0.05) at a threshold concentration of 5mM. Fluoride ion also inhibited Na-K- ATPase activity at 5 mM (-58%, P<0.05). Major morphologic alterations of mitochondria, including crystal formation, were detected from 1 mM fluoride concentration. Time-effect studies showed that, after only 6 h of exposure at 5 mM, fluoride decreased cell number (-13%, P<0.05), (3)H-leucine incorporation (-48%, P<0.05), and Na-K-ATPase activity (- 20%, P<0.05) and increased lactate dehydrogenase release (+145%, P<0.05). Crystal deposits in mitochondria again were a more sensitive marker of cell injury, detectable after only 2 h of exposure. Conclusions these results suggest that the mitochondrion is a target of fluoride toxicity in human collecting duct cells, and its alteration is partly responsible for the sodium and water disturbances observed in patients.

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37

Mosleh, Y. Y., S. F. M. Moussa, and L. H. Y. Mohamed. "Comparative toxicity of certain pesticides to peach fruit fly, Bactrocera zonata Saunders (Diptera: Tephritidae) under laboratory conditions." Plant Protection Science 47, No. 3 (August 9, 2011): 115–20. http://dx.doi.org/10.17221/52/2009-pps.

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Peach fruit fly, Bactrocera zonata (Saunders) (Diptera: Tephritidae), has been a serious pest in the last decade attacking a wide range of fruits in Egypt. The toxicity of Malathion, Diazinon, Methoxyfenozide, and Lufenuron to adult males and females of Bactrocera zonata was studied under laboratory conditions. Diazinon was the most toxic among the tested compounds followed by Malathion, Lufenuron and Methoxyfenozide to Bactrocera zonata at 24 h post treatment, the respective LC50 values were 0.20 ppm, 0.48ppm, 8.97ppm, and 9.73ppm for males and 0.26 ppm, 0.91ppm, 11.26ppm, and 14.12ppm for females. At 48 h post treatment Diazinon was the most toxic followed by Malathion, Methoxyfenozide and Lufenuron to Bactrocera zonata, LC50 values were 0.09ppm, 0.34ppm, 1.60ppm, and 1.88 ppm for males and 0.14 ppm, 0.44ppm, 1.68ppm and 2.17 ppm for females. At 72 h post treatment Diazinon was the most toxic followed by Malathion, Lufenuron and Methoxyfenozide to Bactrocera zonata, LC50 values were 0.02 ppm, 0.13ppm, 0.22ppm and 0.51ppm for males and 0.07 ppm, 0.16ppm, 0.55 ppm and 0.62 ppm for females. It is observed that LC50 values for treated adult females increased more than in the treated adult males at 24 h, 48 h, and 72 h post treatment. It means that the adult males were more susceptible to the tested insecticides than the adult females.

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38

Toukourou, Habib, Francine Uwambayinema, Yousof Yakoub, Birgit Mertens, Anatole Laleye, Dominique Lison, Joelle Quetin-Leclercq, and Fernand Gbaguidi. "In Vitro and In Vivo Toxicity Studies on Cymbopogon giganteus Chiov. Leaves Essential Oil from Benin." Journal of Toxicology 2020 (January 28, 2020): 1–12. http://dx.doi.org/10.1155/2020/8261058.

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Cymbopogon giganteus Chiov. (Poaceae) is a medicinal plant used to treat various diseases in traditional medicine in several African countries. The present study aims to evaluate the oral and inhalation toxicity as well as the mutagenic effects of the essential oil of Cymbopogon giganteus leaves (EOCG) from a sample collected in Benin. Mutagenic potential was assessed by the Ames test using Salmonella typhimurium strains TA98 and TA100. Oral acute toxicity was carried out by administration of a single dose of 2000 mg/kg b.w. to Wistar rats while oral subacute toxicity was assessed by daily administration of 50 and 500 mg/kg of EOCG for 28 days. Finally, inhalation toxicity was assessed by administration of a single dose of 0.125%, 0.5%, 2% or 5% v/v of EOCG emulsions in 0.05% v/v lecithin solution in sterile water for the first experiment, and in a second one by administration of single dose of 0.125% or 0.5% v/v. A broncho-alveolar lavage was performed after 3 h or 24 h, respectively. The results show that EOCG is not mutagenic on Salmonella typhimurium strains at the highest concentration tested (200 μg/plate). In the acute oral toxicity study, EOCG induce neither mortality nor toxicity, showing that the LD50 is greater than 2000 mg/kg. The subacute oral toxicity study at both doses did not show any significant difference in body weight, relative organ weight, hematological and/or biochemical parameters or histopathology as compared to the control group. EOCG induced mortality and inflammation in lungs 3 h after administration of a single dose of 5% or 2% v/v. Single doses of 0.125% or 0.5% v/v did not induce inflammation, cell recruitment nor cytotoxicity in lungs 3 h or 24 h after administration, suggesting safety at these concentrations. This first report on the in vivo toxicity will be useful to guide safe uses of EOCG.

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39

Muangphra, Ptumporn, and Ravi Gooneratne. "Toxicity of Commercial Neem Extract to Earthworms (Pheretima peguana)." Applied and Environmental Soil Science 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/925950.

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The LC50of commercial neem extract (Sadao Thai III containing azadirachtin; NEEM) on filter paper in the earthwormPheretima peguanaat 48 h and 72 h was 3.79 and 3.33 g , respectively. In earthworms exposed to five NEEM concentrations from 0.39 (~10% of 48-h LC50) to 3.13 (~80% of 48-h LC50) g , the radial thickness of the epidermis and body wall significantly () decreased, and thickness of intestinal epithelium increased but only at high doses, approximately 25-fold above the concentration permitted for use as an insecticide in field applications (0.09 g ). NEEM significantly () increased the number of binucleated coelomocytes in the micronucleus test (detects chromosomal aberrations) at 3.13 g , approximately 35-fold higher than the recommended dose, but it did not cause coelomocyte DNA single-strand breaks in the comet assay. Thus, NEEM is cytotoxic (increase in binucleates through the inhibition of cytokinesis) but not genotoxic to earthworm coelomocytes. This study demonstrates that the recommended dosage of commercial neem extract as an insecticide in agricultural practices is safe for earthworms.

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40

Paľove-Balang, P., A. Kisová, J. Pavlovkin, and MistríkI. "Effect of manganese on cadmium toxicity in maize seedlings." Plant, Soil and Environment 52, No. 4 (November 15, 2011): 143–49. http://dx.doi.org/10.17221/3358-pse.

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The interaction of manganese with cadmium (Cd) toxicity was studied on maize plants grown in hydroponics. Manganese supplied as MnSO4clearly alleviated the toxic effect of cadmium on the root growth of maize seedlings. The magnitude of alleviation was dose dependant and total abolition of 10µM Cd toxicity on root growth was observed at Mn/Cd ratio of 20:1. The 12 h pre-treatment with 10μM Cd was generally toxic for nitrate uptake and reduction (both determined in Cd-free media). The beneficial effect of 100μM Mn on this toxicity was confirmed for the low-affinity nitrate uptake system, but on the other hand, Mn alone seems to be slightly toxic for high affinity nitrate uptake system and on the nitrate reductase activity.

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41

Reid, B. L., and G. W. Bennett. "Oral Toxicity of Cockroach Bait Toxins, 1989." Insecticide and Acaricide Tests 17, no. 1 (January 1, 1992): 380. http://dx.doi.org/10.1093/iat/17.1.380.

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Abstract Single feeding assays evaluated the oral toxicity of historic (chlordecone-Kepone and dechlorane-Mirex) and current (abamectin, chlorpyrifos, hydramethylnon, and sulfluramid) bait toxicants against German cockroach nymphs. Toxicants were formulated as diets by finely grinding Wayne Rodent Blox™, and reconstituting 5-g portions with 6 ml of water and 3 ml of acetone solution of the technical material. This media was mixed thoroughly, pressed into plexiglass molds, and allowed to dry for 48 h within an evacuation hood, yielding pelletized diets of a known concentration. Several diet concentrations were provided to groups of 10 unsexed, 2-d old, 5th instars which had been denied food for 72 h. Test insects were housed in 100 × 25 mm vented plastic petri dishes supplied with a water vial and a cardboard harborage. 10 mg of each diet concentration was introduced and after 2 h, when this small portion (i.e., single feeding) was completely consumed, untreated diet was then provided through daily observation of mortality until all insects had died or reached adulthood. Each diet concentration was replicated six times and regression of cumulative probit mortality vs. the Log10 of dosage (extrapolated from diet concentration) estimated lethal doses. These analyses were conducted on data from 2 DAT for those toxicants with an acute action, and on data from approximately 14 DAT, when all survivors had become adults, for toxicants with delayed action.

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42

Howard, R. S., P. StJ Trend, and H. R. A. Townsend. "EEG Appearances in Acute Carbamazepine Toxicity." Human & Experimental Toxicology 9, no. 5 (September 1990): 313–15. http://dx.doi.org/10.1177/096032719000900508.

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A 16-year-old woman deliberately took a large, toxic overdose of carbamazepine and recovered despite a high plasma level. During the acute phase the EEG was dominated by occipital delta activity suggestive of a brainstem disorder. Following 24-h treatment with activated charcoal the plasma carbamazepine was cleared and the EEG returned to normal.

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43

Leonard, B. Roger, and J. B. Graves. "Toxicity of Selected Insecticides, 1988." Insecticide and Acaricide Tests 14, no. 1 (January 1, 1989): 250. http://dx.doi.org/10.1093/iat/14.1.250.

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Abstract Selected insecticide treatments were applied to a field of cotton on the Dean Lee Research Station, Alexandria, La., which had been planted 23 Jun in a silty clay loam soil. Prior to the study, this field had not received an application of insecticide. All insecticides were applied using a hand-held boom with 2 X-3 hollow-cone nozzles/row and charged with a compressed-CO2 spraying system calibrated to deliver 6 gal total spray/acre at 38 psi. Plots consisted of 2 rows (38-inch spacing) by 100 ft arranged in a completely random design and replicated 4 times. Freshly laid white Heliothis spp. eggs (10/plot) were collected from each plot 4, 48, and 72 h after treatment. Eggs (attached to a small piece of foliage) were removed from the plant, individually transferred to rearing media, and held in the laboratory at room temperature (80°F) and a photoperiod of 14:10 (L:D). Mortality to eggs and larvae for each collection was determined 96 h after removal from the field. The survivors in the egg cohort in the untreated control were reared to adults and identified as a population of 64% tobacco budworms and 36% bollworms. Mortality was recorded if eggs did not hatch. Treatment toxicity to newly hatched larvae was determined by the inability of the insect to change position after being prodded. There was no rainfall recorded and relative humidity remained low during the study.

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44

Liu, Yufu, Guodong Yang, Chunqi Yang, Zhuo Shi, Yi Ru, Ningning Shen, Chengrong Xiao, Yuguang Wang, and Yue Gao. "The Mechanism of Houttuynia cordata Embryotoxicity Was Explored in Combination with an Experimental Model and Network Pharmacology." Toxins 15, no. 1 (January 13, 2023): 73. http://dx.doi.org/10.3390/toxins15010073.

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Houttuynia cordata (H. cordata) is the most common herb as a food and traditional Chinese medicine. Currently, studies on its toxicity have mainly focused on hepatotoxicity. However, its potential embryotoxicity by long-term exposure is often overlooked. Objective: To investigate the effects of H. cordata on embryonic development and its toxicity mechanism by combining network pharmacology, molecular docking, and in vitro experimental methods. Methods: The effects of H. cordata on embryos were evaluated. Zebrafish embryos and embryoid bodies were administered to observe the effects of H. cordata on embryonic development. Based on network pharmacological analysis, it was found that the main active agents producing toxicity in H. cordata were oleanolic acid, lignan, and aristolactam AII. H. cordata can affect PI3K-Akt, MAPK, and Ras signaling pathways by regulating targets, such as AKT1, EGFR, CASP3, and IGF-1. RT-PCR and immunohistochemistry results showed that the expression of AKT1 and PI3K in the embryoid body was significantly reduced after drug administration (p < 0.05). Conclusions: The results of network pharmacology and in vitro experiments suggest that H. cordata may affect embryonic development by influencing the PI3K-Akt signaling pathway.

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45

Stohs, S. "Oxidative mechanisms in the toxicity of metal ions." Free Radical Biology and Medicine 18, no. 2 (February 1995): 321–36. http://dx.doi.org/10.1016/0891-5849(94)00159-h.

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KERSTENS, P. "5-nucleotidase and azathioprine-related bone-marrow toxicity." Lancet 342, no. 8881 (November 1993): 1245–46. http://dx.doi.org/10.1016/0140-6736(93)92231-h.

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47

Messiha, F. S. "Maternally-mediated developmental lithium toxicity in the mouse." General Pharmacology: The Vascular System 24, no. 1 (January 1993): 9–15. http://dx.doi.org/10.1016/0306-3623(93)90004-h.

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48

Thakkar, Nalin S., and Christopher S. Potten. "Abrogation of adriamycin toxicity in vivo by cycloheximide." Biochemical Pharmacology 43, no. 8 (April 1992): 1683–91. http://dx.doi.org/10.1016/0006-2952(92)90697-h.

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49

Sies, H., and H. de Groot. "Role of reactive oxygen species in cell toxicity." Toxicology Letters 64-65 (December 1992): 547–51. http://dx.doi.org/10.1016/0378-4274(92)90230-h.

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50

Qureshi, S., A. H. Shah, M. Tariq, and A. M. Ageel. "Studies on Herbal Aphrodisiacs Used in Arab System of Medicine." American Journal of Chinese Medicine 17, no. 01n02 (January 1989): 57–63. http://dx.doi.org/10.1142/s0192415x89000103.

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Abstract:

Toxictity studies were conducted on Brassica rapa, Prunus amygdalus and Zingiber officinale, used as aphrodisiacs in Arab Medicine. During acute toxicity test observations were made for 24 h where all these plants showed no toxicity. The animals were tested for 3 months in chronic treatment. External morphological changes, visceral toxicity, haematological changes, effects on average body weight, vital organ weight, sperm contents, sperm motility and sperm abnormalities were recorded. The average body weight increase was significant in B. rapa and P. amygdalus treated animals. Haematological studies revealed reduction in WBC level in these groups. These changes were not significant in Z. officinale treated animals. In all three groups the visceral condition was normal and the percent lethality was insignificant as compared to the control. All these plant extracts significantly increased the sperm motility and sperm contents in the epididymides and vas deferens without producing any spermatotoxic effect.

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Journal articles on the topic 'H+ toxicity'

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