Biochemical effect

Research on the biochemical effects of 03 has been extensive. Among the many mechanistic postulations that have been advanced concerning the toxicity of 03, the following are noted (1) reactions with proteins and amino acids (2) reactions with lipids (3) formation of free radicals (4) oxidation of sulfhydryl compounds and pyridine nucleotides (5) influence on various enzymes and (6) production of more or less nonspecific stress, with the release of histamine. 

Balchum et al. (1971) have provided evidence supporting the concept that the peroxidation or ozonization of unsaturated fatty acids in biological membranes is a primary mechanism of the deleterious effects of 03. The hypothesis is based on the tendency of 03 to react with the ethylene groups of unsaturated fatty acids, resulting in the formation of free radicals. The free radicals can, in the presence of molecular oxygen, cause peroxidation of unsaturated fatty acids. In support of this hypothesis is the evidence that after 03 exposure there was a relative decrease in unsaturated fatty acids as compared to saturated fatty acids, and the more unsaturated the fatty acid, the greater the loss. Furthermore, a deficiency of vitamin E increases the toxicity of 03 for the rat (Goldstein et al. 1970). 

Another chemical pathway leading to 03-dependent unsaturated fatty acid oxidation is through incorporation of 03 into the fatty acid double 

Lanthanides have high electrostatic affinity for Ca binding sites, most likely due to their shared properties such as ionic size and charge density. Thus, lanthanides could compete for, or displace, Ca from 

Some lanthanides have been reported to exhibit antitumor activity both in vitro and in vivo. The activity of sarcomas in rats and lymphatic leukemia and lymphosarcomas in mice was inhibited by La (Hisada 

GdClj has been used to study the mechanisms of chemical-induced hepatotoxicity (Badger et al. 1997, Sauer et al. 1997). Since lanthanides have an affinity for reticuloendothelial cells, GdClj injection selectively destroys Kupffer cells (the resident macrophage cell in the liver), and this results in protection of the liver from a number of toxicants hence, a role is suggested for these cells in chemical-mediated hepatotoxicity. The role of Kupffer cells in hepatotoxicity was implicated for those compounds required to undergo biotransformation before eliciting their toxicity (e.g., 1,2-dichlorobenzene and carbon tetrachloride), as well as those chemicals which do not (e.g., cadmium chloride). 

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W. Rademacher, "Biochemical Effects of Plant Growth Retardants," in Plant Biochemical Regulators, Marcel Dekker Inc, New York, 1991. 

Commercial PCBs Toxic and Biochemical Effects. PCBs and related halogenated aromatic hydrocarbons ehcit a diverse spectmm of toxic and biochemical responses in laboratory animals dependent on a number of factors including age, sex, species, and strain of the test animal and the dosing regimen (single or multiple) (27—32). In Bobwhite and Japanese quad, the LC q dose for several different commercial PCB preparations ranged from 600 to 30,000 ppm in the diet the LC q values for mink that were fed Aroclors 1242 and 1254 were 8.6 and 6.7 ppm in the diet, respectively (8,28,33). The... 

Senior, A.E. Shenatt, H.S.A. (1968). Biochemical effects of the hypoglycaemic compound pent-4-enoic acid and related non-hypoglycemic fatty acids. Oxidative phosphorylation and mitochondrial oxidation of pyruvate, 3-hydroxybutyrate and tricarboxylic acid-cycle intermediates. Biochem. J. 110,499-509. 

This tendency to interact with -SH groups appears to be the fundamental chemical reaction behind most of the adverse biochemical effects of organomercury compounds it is also the basis for one mechanism of detoxication. 

CBs, like OPs, can cause a variety of sublethal neurotoxic and behavioral effects. In one study with goldfish Carrasius auratus), Bretaud et al. (2002) showed effects of carbofuran on behavioral end points after prolonged exposure to 5 pg/L of the insecticide. At higher levels of exposure (50 or 500 pg/L), biochemical effects were also recorded, including increases in the levels of norepinephrine and dopamine in the brain. The behavioral endpoints related to both swimming pattern and social interactions. Effects of CBs on the behavior of fish will be discussed further in Chapter 16, Section 16.6.1. 

Aldridge, W.N. and Street, B.W. (1964). Oxidative phosphorylation biochemical effects and properties of trialkyl tin. Biochemical Journal 91, 287-297. 

Eaton S et al Multiple biochemical effects in the pathogenesis of fatty liver. EurJ Clin Invest 1997 27 719. 

Nishikawa, Y., Minenaka, Y, and Ichimura, M., Physiological and biochemical effects of carotenoid (P-carotene and astaxanthin) on rat, Koshien Daigaku Kiyo, 25, 19, 1997 [in Japanese]. 

In recent years it has been realized that molecular modeling studies of the alkaloidal molecules having different pharmacological activities are highly important in order to explain their mechanisms, at least partially in some cases. This chapter presents and critically reviews some examples of molecular modeling studies of alkaloids, based on their different biological properties or sometimes performed in parallel to explain their biochemical effects. 

Rudneva-Titova I. 1998. The biochemical effects of toxicants in developing eggs and larvae of Black Sea fish species. Mar Environ Res 46 499-500. 

Ross, S.B. Ogren, S.O. and Renyi, L. Antagonism of the acute and longterm biochemical effects of 4-chloroamphetamine on the 5-HT neurons in rat brain by inhibitors of the 5-hydroxytryptamine uptake. Acta Pharmacol Toxicol [Copenh] 39 456-476, 1976. 

Sekerke, HJ. Smith, Fl.E. Bushing, J.A. and Sanders-Bush, E. Correlation between brain levels and biochemical effects of the optical isomers of /)-chloroamphetamine. J Pharmacol Exp Ther 193 835-844, 1975. 

The problem with the neural-plasticity hypothesis is that it does not explain how all of these very different treatments -including drugs that are supposed to have biochemical effects that are directly opposite to each other - produce their hypothesized effects on neural networks. In seeming to explain so much, the neural-plasticity hypothesis (at least as it is used as an explanation of antidepressant treatment) may actually explain nothing at all. And if placebos produce changes in neural plasticity, why bother with antidepressant drugs ... 

Savolainen H, Tenhunen R, Elovaara E, et al. 1980. Cumulative biochemical effects of repeated subclinical hydrogen sulfide intoxication in mouse brain. Int Arch Occup Environ Health 46 87-92. 

Torrans EL, Clemens HP. 1982. Physiological and biochemical effects of acute exposure of fish to hydrogen sulfide. Comp Biochem Physiol C 71 183-190. 

Cory-Slechta DA. 1990b. Lead exposure during advanced age Alterations in kinetics and biochemical effects. Toxicol Appl Pharmacol 104 67-78. 

Lara-Lemus A., Drucker-Colin R., Mendez-Franco J., Palomero-Rivero M., Perez de la Mora M. (1998). Biochemical effects induced by REM sleep deprivation in naive and in D-amphetamine treated rats. Neurobiology 6(1), 13-22. 

Rivera-Pastrana DM, Bejar AAG, Martinez-Tellez MA, Rivera-Dominguez M and Gonzalez-Aguilar GA. 2007. Postharvest biochemical effects of UV-C irradiation on fruit and vegetables. Revista Fitotecnia... 

Since the tragic human exposure to diethyltin salts for the therapy of an infectious skin disease by Staphylococcus in France in the 1950s, the toxic and biochemical effects of many of these derivatives have been explored. Di- and tri-ethyltin salts have been demonstrated to have pronounced effects on intermediary metabolism in brain and liver. These effects have been suggested to be due to inhibition of the mitochondrial functions9,27. 

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