Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Toxicity, mechanisms animal data

Based upon the available data, derivation of AEGL-1 values was considered inappropriate. The continuum of arsine-induced toxicity does not appear to include effects consistent with the AEGL-1 definition. The available human and animal data affirm that there is a very narrow margin between exposures that result in little or no signs or symptoms of toxicity and those that result in lethality. The mechanism of arsine toxicity (hemolysis that results in renal failure and death), and the fact that toxicity in humans and animals has been reported at concentrations at or below odor detection levels (-0.5 parts per million (ppm)) also support such a conclusion. The use of analytical detection limits (0.01 to 0.05 ppm) was considered as a basis for AEGL-1 values but was considered to be inconsistent with the AEGL-1 definition. [Pg.85]

Reference The available human and animal data indicate that there is very little margin between seemingly inconsequential exposures and lethal exposures. The mechanism of arsine toxicity (hemolysis and subsequent renal failure) and the fact that toxicity has been demonstrated at or below the odor threshold justify the inappropriateness of AEGL-1 values for any exposure period. [Pg.127]

Between October 30 and November 4, 2000, 11 persons were intoxicated due to ingestion of a serranid fish Epinephelus sp. in Kochi Prefecture, Japan. Their symptoms included severe muscle pain, low back pain, and discharge of black urine. The causative agent was identified as palytoxin on the basis of delayed haemolytic activity, which was inhibited by an anti-palytoxin antibody and ouabain (Taniyama et al. 2002). Although the toxic dose of palytoxin in humans could not be determined, extrapolation of the data available in animals will give a toxic dose in a human of about 4 pg. This fact places palytoxin among the most toxic nonproteinic animal toxins known to date (Taniyama et al. 2002) however, its mechanisms of toxicity remain to be elucidated. [Pg.104]

The opportunity to reduce the uncertainties regarding animal data and the broader questions of the role of environmental chemicals in human cancer and other diseases is at hand. Toxicologists are more frequently turning to the study of the mechanisms underlying the biological actions of carcinogens and other toxicants, and we now turn to this topic, to clarify some matters covered in the present chapter and to prepare the way for our later discussions of dose—response and human risk. [Pg.85]

The first type concerns the hazards of these chemicals their flammability, their explosivity, their radioactivity, and their toxicity. In the present context we are interested in the toxic properties of these chemicals. So, it would be necessary, under what is called the hazard evaluation step of risk assessment, to assemble all the available epidemiology and experimental toxicity data (the latter to include animal toxicity studies, ADME data, and studies of mechanisms of toxic action). The assembled data would then be critically evaluated to answer the question what forms of toxicity can be caused by the chemical of interest, and how certain can we be that human beings will be vulnerable to these toxic effects (under some conditions) ... [Pg.246]

The immunosuppressive drug cyclosporine A (CSA) has revolutionized transplant medicine. However, CSA induced-nephrotoxicity still represents a major therapeutic challenge. Chronic CSA nephropathy is characterized by a decrease in glomerular filtration rate (GFR), tubular atrophy, interstitial fibrosis and progressive renal dysfunction. It is difficult to delineate the mechanisms of CSA toxicity from clinical data since the majority of clinical experiences with CSA have been in renal transplant recipients. Animal models of CSA nephropathy have brought some insights, how-... [Pg.130]

Biodistribution and safety assessment during preclinical development requires both in vitro and in vivo studies. Biocompatibility of nanoparticles can be determined by in vitro cytotoxicity testing on cell lines. In vitro studies also facilitate the revelation of biochemical mechanisms under controlled conditions not achievable by in vivo studies. The rationale underlying the selection of in vitro assays to provide meaningful efficacy and safety data on nanoparticle is detailed in the literature. However, it is in vivo biodistribution and toxicity studies that determine safety for clinical trials, and all preclinical characterization studies must necessarily include in vivo determination of a nanoparticles biodistribution and toxicity in animal tests. FDA provides detailed guidelines for biodistribution and safety assessment of drug formulations in vivo using animal models and specific consideration for nanoparticle samples are reviewed elsewhere. ... [Pg.100]


See other pages where Toxicity, mechanisms animal data is mentioned: [Pg.86]    [Pg.110]    [Pg.123]    [Pg.125]    [Pg.129]    [Pg.131]    [Pg.128]    [Pg.120]    [Pg.267]    [Pg.433]    [Pg.524]    [Pg.204]    [Pg.179]    [Pg.102]    [Pg.114]    [Pg.256]    [Pg.164]    [Pg.127]    [Pg.772]    [Pg.111]    [Pg.230]    [Pg.2827]    [Pg.42]    [Pg.149]    [Pg.139]    [Pg.79]    [Pg.222]    [Pg.255]    [Pg.457]    [Pg.86]    [Pg.110]    [Pg.123]    [Pg.125]    [Pg.129]    [Pg.131]    [Pg.489]    [Pg.674]    [Pg.563]    [Pg.118]    [Pg.285]    [Pg.686]   
See also in sourсe #XX -- [ Pg.85 ]




SEARCH



Animal toxic data

Animal toxicity

Mechanical data

Toxic mechanisms

Toxicity data

© 2024 chempedia.info