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Journal articles on the topic 'Toxicity'

To see the other types of publications on this topic, follow the link: Toxicity.

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

Hutchings, Matt, Ian Johnson, Elaine Hayes, Andrew E. Girling, John Thain, Kevin Thomas, Rachel Benstead, et al. "Toxicity Reduction Evaluation, Toxicity Identification Evaluation and Toxicity Tracking in Direct Toxicity Assessment." Ecotoxicology 13, no. 5 (July 2004): 475–84. http://dx.doi.org/10.1023/b:ectx.0000035297.90620.73.

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2

Paulíková, I., G. Kováč, J. Bíreš, Š. Paulík, H. Seidel, and O. Nagy. "Iodine toxicity in ruminants." Veterinární Medicína 47, No. 12 (March 30, 2012): 343–50. http://dx.doi.org/10.17221/5845-vetmed.

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The inadequate intake of iodine is still a topical problem, because it contributes to a reduction in performance through the disturbed health of adult animals and their offspring. The necessity of iodine is frequently described in association with hypothyroidal state. In our work we want to assign the hidden risk of prolonged iodine feeding in ruminants. We discuss the possible sources of iodine intoxication, the clinical signs of the intoxication, its effects on production, reproduction, and thyroid functions; animal susceptibility to intoxication; laboratory and necropsy findings; diagnostic, and therapeutic possibilities.

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3

A, Semwal. "Phytotherapy Toxicity in Aquaculture." Advances in Pharmacology and Clinical Trials 8, no. 3 (July 6, 2023): 1–4. http://dx.doi.org/10.23880/apct-16000219.

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The fish disease significantly affects the aquaculture industry and causes economic harm. Antibiotics, chemotherapeutics and other synthetic pharmaceuticals are continuously used by farmers to mitigate infectious diseases. Phytotherapy without side effects is an eco-friendly, socio-economic and modern approach to mitigate disease. Toxicological and pharmacological studies are prerequisites for phytotherapy-related research and help to decide a safe dose for the main experiment and commercial aqua products. In toxicity studies, LD50 and LC50 are reliable and widely used acute toxicity parameters.

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4

HALL, Stephen. "Toxicity." Nephrology 3, s2 (September 1997): s788. http://dx.doi.org/10.1111/j.1440-1797.1997.tb00310.x.

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5

Enara, Mohamed. "Case Report (Acute Iron Toxicity)." Advances in Clinical Toxicology 5, no. 2 (2020): 1–2. http://dx.doi.org/10.23880/act-16000185.

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6

Hussain, Sadique. "Nanotoxicology: Nano Toxicity in Humans." Pharmaceutics and Pharmacology Research 5, no. 1 (January 4, 2022): 01–03. http://dx.doi.org/10.31579/2693-7247/059.

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Nanoparticles (NPs) have attracted a lot of attention in the fields of electronics, biology, and astronautics because of their unique physicochemical and electrical characteristics. NPs are materials with at least one dimension of fewer than 100 nanometres that are commercially manufactured (Bahadar et al., 2016; Vishwakarma et al., 2010). In the medical field, drugs, proteins, DNA, and monoclonal antibodies are all being delivered via NPs(Hussain et al., 2021).

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7

Quimby, Alexandra Elizabeth, and Rajeev Sachdeva. "Lithium Toxicity at Therapeutic Blood Levels: A Case Report." University of Ottawa Journal of Medicine 5, no. 2 (November 2, 2015): 26–28. http://dx.doi.org/10.18192/uojm.v5i2.1368.

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ABSTRACT:This report describes a case of lithium toxicity occurring at therapeutic blood levels in a 47-year-old man with bipolar disorder and a history of alcohol abuse. We discuss the clinical presentation of lithium toxicity, as well as factors that may contribute to a reduction in the blood levels required for the precipitation of toxic effects. In addition, we review the literature on cases of lithium toxicity occurring at therapeutic blood levels, including diagnosis and management thereof.RÉSUMÉ:Ce rapport décrit un cas de toxicité au lithium se produisant à des niveaux sanguins thérapeutiques chez un homme de 47 ans avec un trouble bipolaire et une histoire d’abus d’alcool. Nous discutons la présentation clinique de toxicité au lithium, ainsi que les facteurs pouvant contribuer à une réduction des niveaux sanguins nécessaires à la précipitation des effets toxiques. En outre, nous passons en revue la littérature sur les cas de toxicité au lithium se produisant à des niveaux sanguins thérapeutiques, y compris son diagnostic et sa gestion.

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8

Usman, A., M. U. Kawu, M. Shittu, N. B. Ibrahim, and A. A. Yahaya. "Synergistic ameliorative effect of ascorbic acid and Moringa oleifera in lead-induced toxicity: a review." Nigerian Journal of Animal Production 50, no. 3 (May 14, 2024): 86–97. http://dx.doi.org/10.51791/njap.v50i3.4031.

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This review is aimed at discussing the synergism between Moringa oleifera and ascorbic acid in lead poisoning. Lead is one of the heavy metals that is ubiquitous in nature and has various industrial applications. This is because of its advantageous physical properties. Although its use has been phased out in some industrial applications such as paints in developed countries, it remains a widely used heavy metal in the developing world. Lead toxicity accounts for thousands of deaths annually. Children are mostly affected by serious outcomes such as permanent neurocognitive damage. A literature search was conducted using ScienceDirect, PubMed, MDPI, Wiley, and Springer. Keywords used for search include “Moringa oleifera” “Ascorbic acid” “Lead toxicity” “Medicinal preparations” “Nutraceuticals” and “Chinese herbal medicine”. Oxidative stress was the major mechanism underlying Pb toxicity. Oxidative stress causes the depletion of endogenous antioxidant systems. Both Moringa oleifera and ascorbic acid have antioxidant properties. This has made it possible for these two agents to be used for treating various ailments, including Pb toxicity. Previous findings have shown a probable synergism between Moringa oleifera and ascorbic acid in ameliorating Pb-induced toxicity. This study indicates that a combined treatment approach comprising of Moringa oleifera and ascorbic acid could provide the best solution for managing Pb-induced toxicity. The classical management for Pb toxicity is chelation therapy, which is usually accompanied by serious side effects. Hence, there is a need for the deployment of nutraceuticals and other plant-derived substances for the better management of Pb toxicity Cette revue vise à discuter de la synergie entre le Moringa oleifera et l'acide ascorbique dans le saturnisme. Le plomb est l'un des métaux lourds omniprésent dans la nature et qui a diverses applications industrielles. Cela est dû à ses propriétés physiques avantageuses. Bien que son utilisation ait été progressivement abandonnée dans certaines applications industrielles telles que les peintures dans les pays développés, il reste un métal lourd largement utilisé dans les pays en développement. La toxicité du plomb est responsable de milliers de décès chaque année. Les enfants sont principalement touchés par des conséquences graves telles que des dommages neurocognitifs permanents. Une recherche documentaire a été menée à l'aide de ScienceDirect, PubMed, MDPI, Wiley et Springer. Les mots clés utilisés pour la recherche incluent « Moringa oleifera », « Acide ascorbique », « Toxicité au plomb », « Préparations médicinales », « Produits nutraceutiques » et « Plantes médicinales chinoises ». Le stress oxydatif était le principal mécanisme sous-jacent à la toxicité du plomb. Le stress oxydatif entraîne l'épuisement des systèmes antioxydants endogènes. Le Moringa oleifera et l'acide ascorbique ont tous deux des propriétés antioxydantes. Cela a permis à ces deux agents d'être utilisés pour traiter diverses affections, notamment la toxicité du plomb. Des découvertes antérieures ont montré une synergie probable entre le Moringa oleifera et l'acide ascorbique pour améliorer la toxicité induite par le Pb. Cette étude indique qu'une approche thérapeutique combinée comprenant du Moringa oleifera et de l'acide ascorbique pourrait constituer la meilleure solution pour gérer la toxicité induite par le Pb. La prise en charge classique de la toxicité du Pb est la thérapie par chélation, qui s'accompagne généralement d'effets secondaires graves. Il est donc nécessaire de déployer des nutraceutiques et d'autres substances d'origine végétale pour une meilleure gestion de la toxicité du plomb.

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9

Messinger, Horst, and Albert Bär. "Subchronic toxicity, toxicity to reproduction and prenatal developmental toxicity of vinyl laurate." Regulatory Toxicology and Pharmacology 70, no. 1 (October 2014): 80–86. http://dx.doi.org/10.1016/j.yrtph.2014.06.015.

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10

Pumpaisalchai, W., S. Kaewvichit, S. Siriaunkgul, T. Taesothikul, W. Niwatananun, and K. Sanichwankul. "TOXICITY OF BARAKOL: HEPATOTOXICITY AND SUBACUTE TOXICITY." Acta Horticulturae, no. 679 (February 2005): 157–63. http://dx.doi.org/10.17660/actahortic.2005.679.19.

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11

Lémery, Emmanuelle, Stéphanie Briançon, Yves Chevalier, Claire Bordes, Thierry Oddos, Annie Gohier, and Marie-Alexandrine Bolzinger. "Skin toxicity of surfactants: Structure/toxicity relationships." Colloids and Surfaces A: Physicochemical and Engineering Aspects 469 (March 2015): 166–79. http://dx.doi.org/10.1016/j.colsurfa.2015.01.019.

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12

Malton, Samuel Robert. "Assessing the risk of chemotherapy toxicity and hospital admission due to toxicity." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14508-e14508. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14508.

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e14508 Background: Acute chemotherapy toxicity can have negative effects for the patient and the health economy. Finding overall toxicity incidence for a typical teaching hospital population proved difficult, although the 2008 report in to deaths within 30 days of chemotherapy found that 43% of patients who died reported a grade 3 or 4 toxicity1. At Nottingham University Hospitals (NUH) a Cancer Admissions and Triage Team was established, who undertake a proactive telephone toxicity assessment 24 hours following the administration of a first cycle of chemotherapy. This had the aim of reducing hospital admission due to toxicity through timely advice and intervention and allowed the accrual of data regarding reported toxicity. Methods: Data was obtained from the telephone assessment of acute toxicity 24 hours after administration of a first cycle of chemotherapy, once the service had been in use for 1 year. Descriptive statistics were produced to establish toxicity incidence and severity and hospital admission rates as well as length of stay. Regression modelling was used to identify predictors of the four outcome measures. The commonest toxicities were explored as secondary outcome measures. Results: 1539 patients were studied and the overall incidence of toxicity was 35.6%. Disease site and number of chemotherapy agents given were shown to predict toxicity, with breast and upper gastrointestinal cancers having a higher likelihood of toxicity. The more anticancer agents used, the higher the risk of toxicity. Disease was predictive of toxicity grade, with urology, gynaecology and lung patients experiencing higher grades of toxicity than other tumour sites. The rate of hospital admission due to toxicity was 13.1% and median length of stay 3 days. The risk of admission had some risk factors in common with toxicity. Disease and the number of drugs in the regimen affected the risk of admission, with gynaecology, head and neck and lung patients and patients who received 3 drugs having a higher likelihood of admission. No predictors could be reliably identified for length of stay. Predictors in the sub-groups of breast, lower gastrointestinal and lung cancers did not differ greatly from the whole population and the number of drugs was shown to be a predictor of nausea, vomiting and fatigue when explored as secondary outcomes. Conclusions: Predictors were identified for occurrence of toxicity, severity of toxicity, risk of hospital admission but not for length of stay. Sub-group analyses were undertaken. The overall burden of acute chemotherapy toxicity of a heterogeneous population was elucidated.

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13

kulkarni, Dr Sameer. "Acute Paracetamol Toxicity - A Case Report." Indian Journal of Applied Research 3, no. 12 (October 1, 2011): 466–68. http://dx.doi.org/10.15373/2249555x/dec2013/142.

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14

S.Soujanya, S. Soujanya, and Karan Rajendra Kharde. "Atrazine induced toxicity in lab animals." Indian Journal of Applied Research 3, no. 7 (October 1, 2011): 637–38. http://dx.doi.org/10.15373/2249555x/july2013/200.

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15

Bhattacharjee, Parmita, and Suchismita Das. "Toxicity of Pesticide Deltamethrin to Fish." Indian Journal of Applied Research 4, no. 5 (October 1, 2011): 19–21. http://dx.doi.org/10.15373/2249555x/may2014/6.

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16

Sharma, Kratika, Indranil Das, Pankaj Jhaldiyal, and Akshat Kumar. "Naphthalene Toxicity-Winter Poison in Teenager." Indian Journal of Emergency Medicine 4, no. 2 (June 15, 2018): 160–61. http://dx.doi.org/10.21088/ijem.2395.311x.4218.17.

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Introduction: Naphthalene is bicyclic aromatic hydrocarbon most commonly used as insect and moth repellent household product for storing clothes. The toxic manifestations have been proposedly due to increased free radical formation leading to lipid peroxidation and formation of epoxide and further ultimate DNA damage. Naphthalene toxicity manifests at doses ranging 5 to 15 gms to incidences as low as 2 gm have been reported in children.

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17

Mehlman, Myron A. "MTBE Toxicity." Environmental Health Perspectives 104, no. 8 (August 1996): 808. http://dx.doi.org/10.2307/3432923.

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18

Fraiser, Lucy H., Sarathchandra Kanekal, and James P. Kehrer. "Cyclophosphamide Toxicity." Drugs 42, no. 5 (November 1991): 781–95. http://dx.doi.org/10.2165/00003495-199142050-00005.

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19

Millichap, J. Gordon. "Valproate Toxicity." Pediatric Neurology Briefs 2, no. 8 (August 1, 1988): 60. http://dx.doi.org/10.15844/pedneurbriefs-2-8-6.

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20

Millichap, J. Gordon. "Carbamazepine Toxicity." Pediatric Neurology Briefs 4, no. 4 (April 1, 1990): 31. http://dx.doi.org/10.15844/pedneurbriefs-4-4-10.

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21

Millichap, J. Gordon. "Valproate Toxicity." Pediatric Neurology Briefs 4, no. 4 (April 1, 1990): 32. http://dx.doi.org/10.15844/pedneurbriefs-4-4-11.

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22

Boisseau, J. "Relay Toxicity." Drug Metabolism Reviews 22, no. 6-8 (January 1990): 685–97. http://dx.doi.org/10.3109/03602539008991463.

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23

Dolinak, David. "Opioid Toxicity." Academic Forensic Pathology 7, no. 1 (March 2017): 19–35. http://dx.doi.org/10.23907/2017.003.

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In recent years, there has been a substantial increase in opioid use and abuse, and in opioid-related fatal overdoses. The increase in opioid use has resulted at least in part from individuals transitioning from prescribed opioids to heroin and fentanyl, which can cause significant respiratory depression that can progress to apnea and death. Heroin and fentanyl may be used individually, together, or in combination with other substances such as ethanol, benzodiazepines, or other drugs that can have additional deleterious effects on respiration. Suspicion that a death is drug-related begins with the decedent's medical and social history, and scene investigation, where drugs and drug paraphernalia may be encountered, and examination of the decedent, which may reveal needle punctures and needle track marks. At autopsy, the most significant internal finding that is reflective of opioid toxicity is pulmonary edema and congestion, and frothy watery fluid is often present in the airways. Various medical ailments such as heart and lung disease and obesity may limit an individual's physiologic reserve, rendering them more susceptible to the toxic effects of opioids and other drugs. Although many opioids will be detected on routine toxicology testing, more specialized testing may be warranted for opioid analogs, or other uncommon, synthetic, or semisynthetic drugs.

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24

Webster, Deacon Gregory. "Financial Toxicity." National Catholic Bioethics Quarterly 18, no. 2 (2018): 227–36. http://dx.doi.org/10.5840/ncbq201818223.

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25

Bryan, Charles L., and Stephen G. Jenkinson. "Oxygen Toxicity." Clinics in Chest Medicine 9, no. 1 (March 1988): 141–52. http://dx.doi.org/10.1016/s0272-5231(21)00490-1.

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26

Groleau, Georgina. "Lithium Toxicity." Emergency Medicine Clinics of North America 12, no. 2 (May 1994): 511–31. http://dx.doi.org/10.1016/s0733-8627(20)30440-5.

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27

Biggi, Gianluca, Elisa Giuliani, Arianna Martinelli, and Emilio Benfenati. "Patent Toxicity." Research Policy 51, no. 1 (January 2022): 104329. http://dx.doi.org/10.1016/j.respol.2021.104329.

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28

DeVoll, James R. "Nanoparticle Toxicity." Aviation, Space, and Environmental Medicine 81, no. 2 (February 1, 2010): 152–53. http://dx.doi.org/10.3357/asem.2722.2010.

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29

Lamoreaux, Janelle. "Reproducing Toxicity." Environmental History 26, no. 3 (July 1, 2021): 437–43. http://dx.doi.org/10.1093/envhis/emab014.005.

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30

Rachlis, Anita, and Mary M. Fanning. "Zidovudine Toxicity." Drug Safety 8, no. 4 (April 1993): 312–20. http://dx.doi.org/10.2165/00002018-199308040-00005.

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31

&NA;. "Gastric toxicity." Drugs & Therapy Perspectives 10, no. 4 (August 1997): 12–14. http://dx.doi.org/10.2165/00042310-199710040-00004.

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32

García, Irene, Cecilia Gotor, and Luis C. Romero. "Beyond toxicity." Plant Signaling & Behavior 9, no. 1 (January 2014): e27612. http://dx.doi.org/10.4161/psb.27612.

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33

Wan, Lichuan, and Haiyan Zhang. "Cadmium toxicity." Plant Signaling & Behavior 7, no. 3 (March 2012): 345–48. http://dx.doi.org/10.4161/psb.18992.

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34

Duggal, M. S., M. E. J. Curzon, R. Balmer, J. Roberts, and D. English. "Potential toxicity." British Dental Journal 198, no. 9 (May 2005): 563. http://dx.doi.org/10.1038/sj.bdj.4812338.

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35

&NA;. "Metabolic Toxicity." Oncology Times 29, no. 15 (August 2007): 16. http://dx.doi.org/10.1097/01.cot.0000288346.14295.8f.

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36

Fromer, Margot. "GI Toxicity." Oncology Times 27, no. 14 (August 2005): 15–17. http://dx.doi.org/10.1097/01.cot.0000291709.35168.f2.

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37

Palmer, Biff F., and Deborah J. Clegg. "Salicylate Toxicity." New England Journal of Medicine 382, no. 26 (June 25, 2020): 2544–55. http://dx.doi.org/10.1056/nejmra2010852.

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38

Ward, Natalie C., Gerald F. Watts, and Robert H. Eckel. "Statin Toxicity." Circulation Research 124, no. 2 (January 18, 2019): 328–50. http://dx.doi.org/10.1161/circresaha.118.312782.

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39

Krisanda, Thomas J. "Digitalis toxicity." Postgraduate Medicine 91, no. 6 (May 1992): 273–84. http://dx.doi.org/10.1080/00325481.1992.11701329.

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40

Tappy, Luc, and Bettina Mittendorfer. "Fructose toxicity." Current Opinion in Clinical Nutrition and Metabolic Care 15, no. 4 (July 2012): 357–61. http://dx.doi.org/10.1097/mco.0b013e328354727e.

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41

Striker, Gary E. "Glucose toxicity." Kidney International 59, no. 2 (February 2001): 799–800. http://dx.doi.org/10.1046/j.1523-1755.2001.059002799.x.

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42

Turner, D. "Diamorphine toxicity." Anaesthesia 47, no. 2 (February 1992): 168–69. http://dx.doi.org/10.1111/j.1365-2044.1992.tb02026.x.

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43

&NA;. "Phenelzine Toxicity." Journal of Clinical Psychopharmacology 8, no. 5 (October 1988): 382???383. http://dx.doi.org/10.1097/00004714-198810000-00027.

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44

Smith, Jeanette, and Jes Roberts. "Lithium Toxicity." Psychiatric Services 44, no. 1 (January 1993): 81—a—82. http://dx.doi.org/10.1176/ps.44.1.81-a.

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45

Iacobuzio-Donahue, Christine A., Edward L. Lee, Susan C. Abraham, John H. Yardley, and Tsung-Teh Wu. "Colchicine Toxicity." American Journal of Surgical Pathology 25, no. 8 (August 2001): 1067–73. http://dx.doi.org/10.1097/00000478-200108000-00012.

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46

Sundar, Shyam, and Jaya Chakravarty. "Antimony Toxicity." International Journal of Environmental Research and Public Health 7, no. 12 (December 20, 2010): 4267–77. http://dx.doi.org/10.3390/ijerph7124267.

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47

Rondeau, Edith Studer. "Wisteria toxicity." Journal of Toxicology: Clinical Toxicology 31, no. 1 (January 1993): 107–12. http://dx.doi.org/10.3109/15563659309000378.

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48

Plummer, John L., Geoffrey K. Gourlay, and David A. Cherry. "Norpethidine toxicity." Pain Reviews 8, no. 3-4 (October 1, 2001): 159–70. http://dx.doi.org/10.1191/0968130201pr184ra.

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49

Rossetti, L., A. Giaccari, and R. A. DeFronzo. "Glucose Toxicity." Diabetes Care 13, no. 6 (June 1, 1990): 610–30. http://dx.doi.org/10.2337/diacare.13.6.610.

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50

KUZUYA, Masayuki. "Oxygen toxicity." Mycotoxins 1997, no. 44 (1997): 1–7. http://dx.doi.org/10.2520/myco1975.1997.1.

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