Toxic effects overview

To acquire an overview of methods and examples of some pitfalls in modeling log P, log S, and the toxic effects of compounds... 

This section presents a brief overview of any known mechanisms of metabolism, absorption, distribution, and excretion including substance reactions or physiological processes that lead to or comprise the mechanism(s) of toxic effect. 

Dibromoethane is metabolized to active forms capable of inducing toxic effects by either of two systems-the microsomal monooxygenase system (cytochrome P-450 oxidation) and the cytosolic activation system (glutathione conjugation). Figure 2-3 provides an overview of the metabolism of... 

Statistical analysis is essential In order to gain an overview of the very extensive data collected during such studies and to highlight any underlying trends. This analysis also aids in determining the non-toxic effect level required by regulatory authorities. 

Concomitants Concomitants can be considered impurities present in naturally occurring, nonsynthesized raw materials. They may either present toxic effects, as with arsenic, or be as harmless as chloride ions. An overview of usual concomitants and their limits cited in pharmacopeial compendia are listed in Table 7. 

When cancer is diagnosed, three primary treatment modalities are available surgery, radiation treatment, and cancer chemotherapy. The purpose of this chapter is to describe the basic rationale of cancer chemotherapy and to provide an overview of the drugs that are currently available to treat specific forms of cancer. Rehabilitation specialists will routinely work with patients undergoing cancer chemotherapy. For reasons that will become apparent in this chapter, these drugs tend to produce toxic effects that directly influence physical therapy and occupational therapy procedures. Therefore, this chapter should provide therapists with a better understanding of the pharmacodynamic principles and beneficial effects, as well as the reasons for the potential adverse effects of these important drugs. 

Adequate extrapolation of results from standard laboratory toxicity tests to other time scales of exposure and response requires observations on the time course of toxic effects. These observations can then be used to construct time-to-event models, such as the DEBtox model mentioned above. These models explicitly address both intensity and duration of exposure to hazardous chemicals, and better use is made of the data gathered from toxicity experiments. Diverse endpoints in time can be addressed, and individual organism characteristics and/or environmental circumstances (e.g., temperature) can be incorporated as covariables. An overview of time-to-event models and approaches and their use in the risk assessment of chemicals is provided by Crane et al. (2002). 

S.C. Smolinske, et al., Toxic effects of nonsteroidal anti-inflammatory drugs in overdose An overview of recent evidence on clinical effects and dose-response relationship. Drug Safety 5 252-274, 1990. 

This entry provides an overview of the anatomy and physiology of the GI system and later describes the type of toxic effects that can be observed with different classes of agents. 

This article describes the structure and function of the musculoskeletal system and provides an overview of the categories of toxic effects that can affect this body system. The article is divided into two principle parts, which form the main components... 

In the following chapter, we introduce HCI assay methods which can be used to identify cytotoxicity, other drug-induced specific toxicologically relevant events, as well as assays for the assessment of cellular morphology and functions. An overview of cellular features associated with potential toxic effects for which specific assays can be applied are shown in Fig. 1. Microscopy images selected from assays are shown in Fig. 2. 

Provides an overview of recognized threats and their toxic effects... 

This chapter presents an overview of the toxic effects associated with inhalation of a nerve agent vapor or aerosol. Many of the studies cited were conducted at the U.S. Army Chemical Biological Center from the 1950s up to the present day. One of the objectives of these studies was to... 

In this chapter, an overview of the development and use of matrix population models for estimation of toxicant effects is presented. Matrix models are one of the modeling approaches that can be used to determine whether populations of organisms will remain the same, increase, or decline, and thus have great potential for use in ecological risk assessment. 

Paraquat and diquat exert their toxic effects in plants mainly by interacting with photos mthesis, and in animals (and, but probably to a much lesser extent, also in plants) by interacting with mitochondrial respiration. A detailed description of the processes of photosynthesis and mitochondrial respiration would require many pages and is beyond the scope of this book. However, as they are key to the discussion, the following paragraphs have been included to provide a brief overview which is summarised in Figure 2. If the reader is interested in a more detailed account, this can be obtained from any standard biochemistry textbook. 

Ultrasound guidance for nerve blocks has revolutionized LRA, and has become state of the art (www.nice.org.uk 2009). Precise identification of nerve structures minimizes risk of inadvertent vessel injury, intravascular injection and complicating hematoma. It improves block success, allows reducing LA dose and dose-related toxic effects [16, 17]. Table 3 gives an overview of maximum recommended dose of LA. 

Because of the toxicity of lead, special care must be taken when working with lead ahoys. Lead and its inorganic compounds are neurotoxias which may produce peripheral neuropathy. Eor an overview of the effects of lead exposure, see Occupational Exposure to Lead, Appendix A (29 CRE 1910.1025) (see... 

It is important to remember that some materials of low acute toxicity may have a significant potential for producing harmful effects by repeated exposure, and vice versa. This stresses the need for a complete overview of the toxicity of a chemical by acute and repeated exposure in the process of hazard evaluation. 

Acute and Chronic Toxicity. Although chromium displays nine oxidation states, the low oxidation state compounds, -II to I, all require Special conditions for existence and have very short lifetimes in a normal environment. This is also tme for most organ ochromium compounds, ie, compounds containing Cr—C bonds. Chromium compounds that exhibit stabiUty under the usual ambient conditions are limited to oxidation states II, III, IV, V, and VI. Only Cr(III) and Cr(VI) compounds are produced in large quantities and are accessible to most of the population. Therefore, the toxicology of chromium compounds has been historically limited to these two states, and virtually all of the available information is about compounds of Cr(III) and/or Cr(VI) (59,104). However, there is some indication that Cr(V) may play a role in chromium toxicity (59,105—107). Reference 104 provides an overview and summary of the environmental, biological, and medical effects of chromium and chromium compounds as of the late 1980s. 

Stahlmann R, Lode H (2000) Safely overview. Toxicity, adverse effects, and interactions. In Andriole V (ed) Hie Quinolones. 3rd edn. London, Academic Press, pp 397-453... 

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