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Inhalation Toxicity of Metal Particles and Vapors
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Acute toxicity is caused by a relatively large dose of a metal toxicant. The onset of symptoms is sudden, and the intensity of effects rises rapidly and if adequate procedures are not performed to neutralize or remove the toxicant, irreversible damage to tissues and systems may cause death. Chronic poisoning develops gradually following long and continued exposure to relatively small doses. Initially, no symptoms manifest, then there is a gradual onset of symptoms. There may be frequent remissions and recurrences of the symptoms. Many metals act as short-term poisons or toxicants in high doses and as long-term systemic poisons in low doses. Chronic poisoning also represents cumulative effects. A metallic toxicant can develop two different sets of symptoms, one for acute and one for chronic toxicity. Chronic toxicity can be reversed by removal of the toxicant, provided no irreversible damage has been done to vital systems. Groth (1972) found that metal interactions were effective in chronic experiments, with mercury toxicity being alleviated by selenium. Delayed, or latent, toxicity is the condition in which clinical effects are observable only months following exposure to the toxicant. Latent toxicity is exemplified by beryllium and chromium. Cumulative effects may or may not be associated with a build up of the toxicant. For example, there is no cumulative concentration of beryllium in pulmonary tissues in the pulmonary granuloma caused by chronic beryllium toxicity.
Toxicology
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Chronic toxicityThis is commonly associated with renal impairment, dehydration, diuretic or NSAID use and congestive cardiac failure.Clinical manifestations of chronic toxicity include: CNS: mild: tremor, hyper-reflexia, ataxia, muscle weaknessmoderate: rigidity, hypotension, stuporsevere: myoclonus, coma and convulsionsgastrointestinal symptoms are not prominent in chronic toxicity.
Nutritional Disorders/Alternative Medicine
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Toxicity of the fat-soluble vitamins may be caused by diminished urinary excretion of normal body stores, as well as ingestion of excess amounts. Acute vitamin A toxicity can occur after a single large dose. The chronic toxicity of hypervitamimosis A results in pruritus (itching), dry scaly skin, changes in nail and hair texture, bone pain, increased cerebrospinal fluid pressure, and hypercalcemia. Prolonged use of vitamin A, even in therapeutic doses, can cause fatigue, nausea, vomiting, dizziness, irritability, cheilosis (inflammation at the corners of the mouth), and generalized skin desquamation (shedding).
Subacute oral toxicology and toxicokinetics of pterostilbene, a novel Top1/Tdp1 inhibiting anti-tumor reagent
Published in Drug and Chemical Toxicology, 2023
Changcheng Sun, Ying Li, Yutian Zhang, Haoyan Huang, Huili Chen, Jiaqin Chen, Luyao Han, Xiang Chen, Xijing Chen, Yongjie Zhang
The safety profile of resveratrol has been extensively investigated in the past decades (Williams et al. 2009, Movahed et al. 2020). In a clinical trial study conducted in 40 volunteers, resveratrol proved to be safe after 29 daily doses of 0.5 g, 1.0 g, 2.5 g, and 5 g, with only moderate intestinal adverse reactions occurring with the highest doses (2.5 g and 5 g) (Brown et al. 2010). Moreover, experiments conducted on animals showed that daily oral administration of 50, 150, and 500 mg/kg resveratrol for 28 days did not cause severe adverse reactions (Bae et al. 2021). However, it is still uncertain whether long-term consumption of pterostilbene will cause body damage. It is well-accepted that toxicokinetics studies are vital in providing safe dose regimen information for future clinical applications of drug candidates (Regner et al. 2011, Kim et al. 2019). Therefore, this study was designed to study the toxicokinetics of pterostilbene after continuous intragastric administration in Sprague-Dawley (SD) rats for 28 days. UPLC–MS/MS was used to determine the drug concentrations in plasma. Target organs were examined to evaluate potential toxic effects, which results were supportive for further chronic toxicity studies. This is the first study, to the best of our knowledge, that reported the oral subacute toxicity and toxicokinetics of pterostilbene in SD rats.
Ultrasound image-guided gene delivery using three-dimensional diagnostic ultrasound and lipid-based microbubbles
Published in Journal of Drug Targeting, 2022
Daiki Omata, Lisa Munakata, Saori Kageyama, Yuno Suzuki, Tamotsu Maruyama, Tadamitsu Shima, Takumi Chikaarashi, Naoya Kajita, Kohji Masuda, Naoto Tsuchiya, Kazuo Maruyama, Ryo Suzuki
No notable tissue damage was observed with the combination of LB and RSP6-16 in the histochemical and serum biological analyses (Figure 5 and Table 3). The histochemical analysis showed that there was no extravasation of red blood cells, suggesting that the combination of LB and RSP6-16 did not induce haemorrhage. Our results indicate that acute toxicity was not induced by treatment with LB and RSP6-16 because the analysis was performed one day after treatment. In this study, we did not examine the long-term damage and, therefore, could not report on the chronic toxicity, which should be evaluated in future studies. Although the luciferase expression in tissues was evaluated after treatment with LB and RSP6-16, the amount of pDNA delivered in the tissues and the type of cells that the pDNA transfected were unclear. The quantitative evaluation of pDNA in each tissue is important to establish gene delivery system. It is also important to determine the cells to which the gene is delivered because when genes are targeted to work in parenchyma but not endothelial cells, the pDNA distribution should be regulated. Therefore, we also need to evaluate these points in future studies.
Using existing knowledge for the risk evaluation of crop protection products in order to guide exposure driven data generation strategies and minimise unnecessary animal testing
Published in Critical Reviews in Toxicology, 2021
Paul Parsons, Elaine Freeman, Ryan Weidling, Gary L. Williams, Philip Gill, Neil Byron
In most cases, the ADIs/cPADs for the SDHIs are based on histopathological effects in liver and or thyroid and, mean body weight decreases observed in the combined rat chronic toxicity/carcinogenicity study and less frequently the mouse. Occasionally the ADI/cPAD is based on effects on these end points in the 2-generation reproductive toxicity study (inpyrfluxam and isofetamid in the USA and penthiopyrad in the EU). Although we did not collate data from subchronic toxicity studies as part of this exercise, the data sources reviewed indicate that for most SDHIs that cause liver, thyroid and body weight effects in long-term studies, these effects are also seen with sub-chronic dosing in 28 day and 90 day toxicity studies and there appears to be little difference between the NOAELs and LOAELs seen in sub-chronic and chronic toxicity studies (see supplemental data files) suggesting that points of departure could be readily derived from sub-chronic studies with appropriate safety factors used for derivation of the ADI/cPAD. This observation is consistent with other studies comparing sub-chronic and chronic toxicity endpoints which show that a factor of two may be sufficient to extrapolate from one to the other (Guth et al. 2020).