Chlorine clinical effects

Introduction of chlorine or bromine into the 3- and/or 4- positions of the side chain yields more potent compounds in terms of hypotension in rats and dopamine p- hydroxylase inhibition (31. 32). The analog YP-279 (XXXV) is also hypotensive in rats but is said not to affect brain norepinephrine biosynthesis unlike fusaric acid or dibromofusaric acid (33-35). Fusaric acid amide (bupicomide, Sch 10595, XXXVI) is clinically effective at 300 to 1800 mg per day and is said to have hemodynamic effects similar to hydralazine (36. 37). The amide is... 

Kleinfeld M, Messite J, Swencicki R Clinical effects of chlorinated naphthalene exposure. J OccupMed 14 377-379, 1972... 

Several papers have now appeared from Ayerst groups detailing the effects of modifications to the structure of the clinically effective neuroleptic butaclamol (9a). Because transposition of chlorine groups can eliminate cataleptic side effects from other tricyclic neuroleptics (e.g., octoclothepin- doclothepin), a series of chloro derivatives of the... 

Kaufman J, Burkons D Clinical, roentgenological and physiological effects of acute chlorine exposure. Arch Environ Health 23 29-34, 1971... 

This section will describe clinical practice and research concerning methods for reducing toxic effects of exposure to chlorine dioxide or chlorite. However, because some of the treatments discussed may be experimental and unproven, this section should not be used as a guide for treatment of exposures to chlorine dioxide or chlorite. When specific exposures have occurred, poison control centers and medical toxicologists should be consulted for medical advice. Standard texts that discuss treatment of toxicologic emergencies contained no information concerning chlorine dioxide or chlorite. 

Kaufman, J., and D.Burkons. 1971. Clinical, roentgenologic and physiologic effects of acute chlorine exposure. Arch. Environ. Health 23(l) 29-34. 

In general, following acute exposure to chlorinated hydrocarbon insecticides, blood chlorinated hydrocarbon levels are not clinically useful for most compounds it reflects cumulative exposure over a period of months rather than recent exposure. Emesis may be indicated and is most effective if initiated within 30 min postingestion. In addition, an activated char-coal/cathartic may be given. For seizures, diazepam should be administered as an intravenous bolus. Oils should not be given by mouth. Adrenergic amines should not be administered because they may further increase myocardial irritability and produce refractory ventricular arrhythmias. If clothing is contaminated, it should be removed. 

Exposures to single toxic chemicals in and around the house produce many well-known identifiable effects in people. An example of such an effect is respiratory irritation following inhalation of chlorine bleach fumes. Often, individuals develop clinical symptoms that are associated with mixtures of chemicals, for example, headache and dizziness following inhalation of paint fumes containing toluene and glycol ethers. 

Unlike more potent chlorinated alkanes such as carbon tetrachloride or 1,1,2-trichloroethane, it is not clear whether the hepatotoxicity of 1,1,1 -trichloroethane is due to a metabolite or the parent compound (see Section 2.3.5.). If metabolites produced by cytochrome P-450 oxidation or dechlorination are responsible for the hepatotoxicity, administering cytochrome P-450 inhibitors (e.g., SKF-525A) may inhibit the development of toxic effects on the liver. Clinical or animal studies examining the use of such an approach and the possibility of side effects, however, were not located. 

The findings of the chlorinated dibenzo-p-dioxin and dibenzofuran isomers in persons residing in contaminated areas and both measured and calculated levels of these compounds in breast milk in the United States presents a possible cause for concern regarding health effects in the nursing infant. Further study is indicated to determine if there is any real clinical risk at the levels found. 

Techniques that might be used to enhance the far-red/near-IR absorption of ALA-induced PpIX appear to be quite limited. PpIX is very photolabile and is easily converted into photoproducts that include at least one chlorin (known as photoprotoporphyrin) which has been identified as the hydroxyaldehyde chlorin derivative of PpIX [147]. All such photoproducts of PpIX absorb light at wavelengths longer than PpIX itself. For example, the hydroxyaldehyde absorbs strongly in the red in the vicinity of 667 nm, while PpIX absorbs around 635 nm. The relevance of these PpIX photoproducts to ALA-PDT as currently practiced is not yet clear. While it is relatively easy to produce PpIX photoproducts in vitro, their yields and photostability in vivo under conditions of clinical ALA-PDT are difficult to determine [148,149]. If treatment conditions that enhance the yield of ALA-induced PpIX photoproducts can be identified, then it might be possible to increase both the photosensitizing efficiency of ALA-PDT and the effective depth of the treatment field. 

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