Peroxide-induced ethylation

The peroxide-induced ethylation of isobutyl chloride in the presence of 19% hydrochloric acid involved monoethylation at all of the carbon atoms in the molecule (Expt. 23). As might be expected, the chief product was l-chloro-2,2-dimethylbutane, produced via abstraction of the hydrogen atom attached to the tertiary carbon atom. Also formed were l-chloro-2-methylpentane (ethylation at a methyl group) and 3-chloro-2-methylpentane (ethylation at the carbon at< n holding the chlorine atom). Some 1-chlorohexane was also obtained in this case, its formation was undoubtedly due to telomerization of the ethylene with hydrogen chloride rather than by a reaction involving the isobutyl chloride. 

The product formed in largest amount by the hydrochloric acid-promoted and peroxide-induced reaction of isopentyl chloride with ethylene was also that formed by alkylation at the tertiary carbon atom, namely 1-chloro-3,3-dimethylpentane (Ig.) (Expt. 25). The remaining constituents of the reaction product were all obtained in very minor amount and were all alkyl chlorides. Among these were 4-chloro-2-methylhexane (y), 1-chlorohexane (formed by telomerization) and some chlorononanes including 5-chloro-3,3-dimethyl-heptane (3 ) formed by ethylation of 12, 4-chloro-2-methyloctane (15) and l-chloro-3-methyloctane (IT). ... 

It may be concluded that primary alkyl chlorides undergo peroxide-induced, hydrogen chloride-promoted, alkylation with ethylene to yield products formed by alkylation at a tertiary carbon atom, at a penultimate secondary carbon atom, or at a primary carbon atom holding a chlorine atom. In the absence of hydrochloric acid, n-butyl chloride underwent little peroxide-induced reaction with ethylene presumably because hydrogen chloride is necessary for propagating the reaction chain via abstraction of hydrogen from the hydrogen chloride to produce the ethylated product and a chlorine atom which maintains the chain by abstraction from the alkyl chloride. 

In the absence of hydrochloric acid, telomeriration occurred, yielding very high molecular weight telo-mer (Expt. 28). Hanford and Roland (3) found that the benzyl peroxide-induced reaction of dioxane with ethylene at 80 C resulted in products formed by reaction of 54 mols of ethylene per mol of p-dioxane. In Expt. 28 using di-t-butyl peroxide at 130 -140 14 mols of ethyl-... 

Azmi NH, Ismail N, Imam MU, Ismail M (2013) Ethyl acetate extract of germinated brown rice attenuates hydrogen peroxide-induced oxidative stress in hitman SH-SY5Y neuroblastoma cells Role of anti-apoptotic, pro-survival and antioxidant genes. BMC Complement Altern Med 13 177... 

A multiwavelength approach might have been considered as an alternative to chemical derivatisation. Ruddle and Wilson [62] reported UV characterisation of PE extracts of three antioxidants (Topanol OC, Ionox 330 and Binox M), all with identical UV spectra and 7max = 277 nm, after reaction with nickel peroxide in alkaline ethanolic solutions, to induce marked differentiation in different solvents and allow positive identification. Nonionic surfactants of the type R0(CH2CH20) H were determined by UV spectrophotometry after derivatisation with tetrabromophenolphthalein ethyl ester potassium salt [34]. Magill and Becker [63] have described a rapid and sensitive spectrophotometric method to quantitate the peroxides present in the surfactants sorbitan monooleate and monostearate. The method, which relies on the peroxide conversion of iodide to iodine, works also for Polysorbate 60 and other surfactants and is more accurate than a titrimetric assay. 

Photochemically induced epoxidation of tetrafluoroethene by oxygen with improved yields (71-76%, conversion 21-62%) is achieved in the presence of radical generators such as tri-bromofluoromethane, 1,2-dibromotctrafluorocthane, ethyl nitrite or 1 H, /F,5//-octafluoropen-tyl nitrite.36 The oxidation of tetrafluoroethene with oxygen can also be catalyzed with bis(trifluoromethyl)diazene an undistillable viscous oil with peroxide composition is formed initially which can be quantitatively converted into carbonyl fluoride when heated.37-38... 

A neuropathy caused by clioquinol (iodochlorohydroxyquin, chinoform) and enhanced by the formation of a clioquinol ferric chelate which initiates lipid peroxidation, leads to complete degeneration of retinal neuroblasts within a day. Vitamin E has a potent protective action against the effects of the chelate [75]. Peroxidative damage to DNA in rat brain, induced by methyl ethyl ketone peroxide, a potent initiator of lipid peroxidation, was inhibited by addition of vitamin E to the diet of rats [76]. 

Visible light induces hydrogen peroxide formation in ascorbic acid and ethyl eosine solution, and H202 initiates the polymerization of vinyl acetate 74,75). 

The decomposition of acetaldehyde, sensitized by biacetyl, was studied at 499 °C by Rice and Walters , and between 410 and 490 °C by Boyer et al. They found the initial rate to be proportional to the square root of the biacetyl concentration and to the first power of the aldehyde concentration. The chains are initiated by the radicals originating from the decomposition of the biacetyl molecule. The decomposition of acetaldehyde can be induced also by di-r-butyl peroxide (at 150-210 °C, about 10-50 molecules decompose per peroxide molecule added), as well as by ethylene oxide (around 450 °C each added ethylene oxide molecule brings about the decomposition of up to 300 acetaldehyde molecules). For the influence of added diethylether, vinyl ethyl ether, ethyl bromide, and ethyl iodide etc., see Steacie °. 

The effect of solvent on the rate of decomposition of diacyl peroxides has been studied extensively. Data for the decomposition of acetyl peroxide in various solvents at two different temperatures are given in Tables 84 and 85. It is apparent that the rates differ little with solvent variation. The decomposition of diacetyl peroxide in /-butyl alcohol and in ethyl alcohol do show appreciable rate differences, the rate coefficients are 0.31 x 10 and 10.1 x 10 secat 60 °C, respectively . This difference in rate is most likely associated with induced decomposition. Again only a small variation in rate is observed in the decomposition of pro-pionyl and butyryl peroxide with solvent change as seen in Table 86. 

By comparison to peroxides, the azo compounds are generally not susceptible to chemically induced decompositions. It was shown,however, that it is possible to accelerate the decomposition of a,a -azobisisobutyronitrile by reacting it with bis(-)-ephedrine-copper(II) chelate. The mechanism was postulated to involve reductive decyanation of azobisisobutyronitrile through coordination to the chelate. Initiations of polymerizations of vinyl chloride and styrene with a,a -azobisisobutyronitrile coupled to aluminum alkyls were investigated. Gas evolution measurements indicated some accelerated decomposition. Also, additions of large amounts of tin tetrachloride to either a,a -azobisisobutyronitrile or to dimethyl-a,a -azobisis-obutyrate increase the decomposition rates. Molar ratios of [SnCl4]/[AIBN]= 21.65 and [SnCl4]/[MAIB] = 19.53 increase the rates by factors of 4.5 and 17, respectively. Decomposition rates are also enhanced by donor solvents, like ethyl acetate or propionitrile in the presence of tin tetrachloride. ... 

For ethyl methanesulphonate- and Fe -treated rat hepatocytes, the in vivo pretreatment with u-a-tocopherol offered no protection against cell death and lipid peroxidation over a 6 h incubation period (Fariss et al. 2001). In contrast, hepatocytes isolated from rats treated with u-a-tocopheryl succinate were completely protected against ethyl methanesulphonate-induced lipid peroxidation for the entire incubation period, which also resulted in dramatic protection against ethyl methanesulphonate-induced cell death. Similarly, n-a-tocopheryl succinate administration in vivo dramatically protected isolated hepatocytes against Fe-induced cell... 

Diethyl maleate (5 mM) and ethyl methanesul-fonate (35 mM) treatments rapidly depleted cellular reduced glutathione below detectable levels (1 nM/ 10 cells), and induced lipid peroxidation and necrotic cell death in freshly isolated rat hepatocytes (Tirmenstein etal. 2000). In hepatocytes incubated with 2.5 mM diethyl maleate and 10 mM ethyl methanesulfonate, however, the complete depletion of cellular GSH observed was not sufficient to induce lipid peroxidation or cell death. Instead, diethyl maleate- and ethyl methanesulfonate-induced lipid peroxidation and cell death were dependent on increased reactive oxygen species production as measured by increases in dichlorofluorescein fluorescence. The addition of antioxidants (vitamin E succinate and deferoxamine) prevented lipid peroxidation and cell death suggesting that lipid peroxidation is involved in the sequence of events leading to necrotic cell death induced by diethyl maleate and ethyl methanesulfonate. 

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