Carbon tetrachloride destruction

Unlike nitration. 2-amino-4-methylselenazole can be directly bromi-nated, using bromine in carbon tetrachloride solution, to give 2-amino-5-bromo-4-methylselenazole hydrobromide [m.p. 180°C (decomp.)] (19). The free base cannot be isolated. Use of excess of bromine can lead to destruction of the molecule. 

Although direct nitration was not possible, 2-amino-4-methylselena-zole can be directly brominated by treatment with bromine in carbon tetrachloride, the hydrogen bromide salt of 2-amino-4-methyl-5-bromoselenazole, mp 180°C (decomp.) is formed. However, all attempts to obtain the free base from this salt failed and led to complete decomposition. In this bromination, an equivalent quantity of bromine must be used excess also leads to complete destruction of the molecule. From the decomposition products an oily compound can be detected similar to bromoacetone. ... 

Chaudhury S, Mehendale HM. 1991. Amplification of carbon tetrachloride toxicity by chlordecone Destruction of rat hepatic microsomal cytochrome P-450 subpopulation. J Toxicol Environ Health 32(3) 277-294. 

A solution containing DTBN and carbon tetrachloride was irradiated at 313 nm or 366 nm, when charge-transfer absorption, resulted in the efficient destruction of... 

Incineration is an estabhshed process for virtually complete destruction of organic compounds. It can oxidize solid, liquid, or gaseous combustible wastes to carbon dioxide, water, and ash. In the pesticide industry, thermal incinerators are used to destroy wastes containing compounds such as hydrocarbons (e.g., toluene), chlorinated hydrocarbons (e.g., carbon tetrachloride). 

The hepatotoxic effects of carbon tetrachloride have been widely studied in animals. Indeed, carbon tetrachloride is used as a model chemical in many laboratory investigations of the basic mechanism of action of hepatotoxic chemicals. Oral exposure to carbon tetrachloride has been observed to result in a wide spectrum of adverse effects on the liver, the most prominent of which are destruction of the smooth and rough endoplasmic reticulum and its associated enzyme activities (Reynolds and Yee 1968), inhibition of protein synthesis (Lutz and Shires 1978), impaired secretion of triglycerides with resultant fat accumulation (Fischer-Nielsen et al. 1991 Recknagel and Ghoshal 1966 Recknagel and Glende 1973 Waterfield et al. 1991), centrilobular necrosis (Blair et al. 1991 Reynolds and Yee 1968 Waterfield et al. 1991 Waterfield et al. 1991 Weber et al. 1992), and eventually fibrosis and cirrhosis (Allis et al. 1990 Bruckner et al. 1986 Fischer-Nielsen et al. 1991 Weber etal. 1992). 

Cytochrome P-450 from rat or human liver microsome preparations is inactivated when incubated anaerobically with carbon tetrachloride in the presence of NADPH and an oxygen-scavenging system (Manno et al. 1988 1992). Inactivation involved destruction of the heme tetrapyrrolic structure, and followed pseudo first-order kinetics with fast and slow half lives of 4.0 and 29.8 minutes. When compared with rat liver microsomes, the human preparations were 6-7 times faster at metabolizing carbon tetrachloride, and only about one- eighth as susceptible to suicide inactivation (about 1 enzyme molecule lost for every 196 carbon tetrachloride molecules metabolized). 

The relative importance of hepatic microsomal lipid peroxidation versus covalent binding of carbon tetrachloride-derived radicals has been the subject of considerable debate. Since cytochrome P-450 loss has been shown to be related to lipid peroxidation and to covalent binding, each in the absence of the other, both of these early consequences of carbon tetrachloride metabolism may contribute to P-450 destruction. Nevertheless, it is still not clear how these initial events are related to subsequent triglyceride accumulation, polyribosomal disaggregation, depression of protein synthesis, cell membrane breakdown and eventual death of the hepatocytes. Carbon tetrachloride... 

Role of alterations in cellular phospholipid in carbon tetrachloride hepatotoxicity Ca2+-dependent i ncreases i n phospholipid destruction mediated by phospholipase... 

De Toranzo EG, Villarruel MC, Castro JA. 1978b. Early destruction of cytochrome P-450 in testis of carbon tetrachloride poisoned rats. Toxicology 10 39-44. 

Lowrey K, Glende EA, Recknagel RO. 1981a. Destruction of liver microsomal calcuium pump activity by carbon tetrachloride and bromotrichloromethane. Biochemical Pharmacology 30 135-140. 

Costs were found to be contaminant specific. Capital costs are generally proportional to flow rate because the capital cost of the power supply is the most expensive power component. Treatment of perchloroethylene (PCE) required three times more electrical power than treatment of TCE. Destruction of carbon tetrachloride required even more energy, but isopropanol was readily destroyed using very little power (D130756, p. 21). 

Furthermore, initiation of this repair process by prior treatment of an animal with a small sub-toxic dose will afford protection against a second, larger dose. This may be part of the mechanism underlying the tolerance to the hepa to toxicity of carbon tetrachloride as well as the destruction of cytochrome P-450 (see chap. 7). Effects on tissue repair may also be important in interactions between compounds. Thus, exposure to another agent such as phenobarbital may stimulate tissue repair and decrease the eventual toxicity of carbon tetrachloride. 

Figure 7.13 The sequence of events underlying carbon tetrachloride toxicity to the liver cell. Although the process starts in the smooth endoplasmic reticulum at CYP2E1, the destruction spreads throughout the cell.

Tolerance is the modification of the biological effect of a chemical as a result of repeated dosing. For example, repeated dosing with phenobarbital leads to a decrease in the anesthetic effect of the drug as a result of enzyme induction. Giving animals a small dose of carbon tetrachloride renders a second larger dose less toxic. This may be a result of induction of repair processes and destruction of cytochrome P-450 caused by the small first dose. 

In an ESR study of the interaction of oxovanadium(IV) cupferronate with basic organic solvents, it has been shown that the coordination of basic solvent molecules leads to the destruction of the dimeric nature of the complex molecules.109 Parameters of the spin Hamiltonian of the ESR spectra of the adducts thus formed in 15 cases have been correlated with the basicity of the organic solvents. By contrast, VO(cupferronate)2 retains its diamagnetic dimeric form in the frozen solution of non-coordinating solvents such as chloroform, carbon tetrachloride, cyclohexane or benzene. 

Radicals such as CCI3, produced during the oxidation of carbon tetrachloride, may induce lipid peroxidation and subsequent destruction of lipid membranes (Figure 8.3). Because of the critical nature of various cellular membranes (nuclear, mitochondrial, lysosomal, etc.), lipid peroxidation can be a pivotal event in cellular necrosis. 

Boronina T, Klabunde KJ, Sergeev G. Destruction of organohalides in water using metal particles carbon tetrachloride/water reactions with magnesium, tin, and zinc. Environ Sci Technol 1995 29 1511-1517. 

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