Cellular protection

EPC is the endogenous cellular protective mechanism in the heart by which brief periods of ischemia induce protection against infarction due to subsequent longer periods of ischemia. 

The results on the cellular protection against N()2 can be interpreted as the N()2 reacting with the three antioxidants to produce their radicals, with ascorbic acid reacting least efficiently, probably due to the lower reduction potential of its radical. Moreover, Arroyo et al. (1992) reported that NO - and N02 -induced mutations in Salmonella typhimurium TA1535 were inhibited efficiently by P-CAR and tocopherols, but not at all by ascorbic acid. 

As mentioned in Sect. 13.3.6, carotenoids serve mainly as accessory pigments in the light harvesting complexes of the photosynthetic apparatus, and additionally as cellular protection against ROS. Whether carotenoids also act as passive UV-sunscreens is... 

Peroxides, including hydrogen peroxide (H2O2), can damage cells by causing unwanted oxidation reactions. The tripeptide glutathione (GSH) is able to participate in a cellular protection mechanism via its ability to form disulfide bridges. 

The role of GSH in cellular protection (see below) means that if depleted of GSH, the cell is more vulnerable to toxic compounds. However, GSH is compartmentalized, and this compartmentalization exerts an influence on the relationship between GSH depletion or oxidation and injury. The loss of reduced GSH from the cell leaves other thiol groups, such as those in critical proteins, vulnerable to attack with subsequent oxidation, cross-linking, and formation of mixed disulfides or covalent adducts. The sulfydryl groups of proteins seem to be the most susceptible nucleophilic targets for attack, as shown by studies with paracetamol (see chap. 7), and are often crucial to the function of enzymes. Consequently, modification of thiol groups of enzyme proteins, such as by mercury and other heavy metals, often leads to inhibition of the enzyme function. Such enzymes may have critical endogenous roles such as the regulation of ion concentrations, active transport, or mitochondrial metabolism. There is... 

Reed DJ. Mechanisms of chemically induced cell injury and cellular protection mechanisms. In Hodgson E, Smart RC, eds. Introduction to Biochemical Toxicology. 3rd ed. Connecticut Appleton-Lange, 2001. 

Dinkova-Kostova AT, Holtzclaw WD, Kensler TW. 2005. The role of Keapl in cellular protective responses. Chem Res Toxicol 18 1779-1791. 

Meister A. 1994. Glutathione, ascorbate, and cellular protection. Cancer Res 54 1969s-1975s. 

The tripeptide thiol glutathione (L-y-glutamyl-L-cysteinyl-glycine (GSH)) found in virtually all cells functions in metabolism, transport and cellular protection. 

GSH Reduced glutathione (the tripeptide glutamyl-cysteinyl-glycine). Found in most tissue, particularly the liver. Plays a major role in detoxification of electrophiles and cellular protection against oxidative damage. 

Glutathione-Dependent Mechanisms in Chemically Induced Cell Injury and Cellular Protection Mechanisms... 

Compartmentation of glutathione has been demonstrated in that a separate pool of glutathione exist in the cytoplasm from that in the mitochondria (Figure 18.6). The cytosolic pool of glutathione has been characterized in terms of cellular protection (Table 18.1). 

L28. Lymar, S. V., and Hurst, J. K., Carbon dioxide physiological catalyst for peroxynitrite-mediated cellular damage or cellular protectant Chem. Res. Toxicol. 9, 845-850 (1996). 

All the products of the oxidation of heme by heme oxygenase are important physiologically. Biliverdin and its reduction product bilirubin are powerful antioxidants and, at nontoxic concentrations, contribute to cellular protection. CO, the second product, also has potent biologic activities, although it is often... 

The fact that nncleic acids are highly reactive and are thus subject to frequent chemical change, i.e., DNA damage, necessitated the evolntionary selection of mnltiple cellular protective mechanisms in order to snstain life. These mechanisms include multiple ones designed to (1) dispose of free radicals, (2) restore the normal chemistry and nncleotide sequence of damaged DNA (DNA repair), and (3) tolerate persistent DNA damage that threatens the viability of cells as a resnlt of arrested DNA replication or transcription, or becanse of high levels of mutation. 

Lindahl T. DNA lesions generated in vivo by reactive oxygen species, their accumulation and repair. In Advances in DNA Damage and Repair Oxygen Radical Effects, Cellular Protection and Biological Consequences. Dizdaroglu M, Karakaya A, eds. 1999. Plenum Publishers, New York, pp 251-257. 

Loft, S. and Poulsen, H.E. In Karakaya, A. and Dizdaroglu, M. (eds.). Oxygen Radical Effects. Cellular Protection and Biological Consequences. Plenum Press, New York, 1998, pp. 267-281. 

Franklin TB, Krueger-Naug AM, Clarke DB, Arrigo AP, Currie RW. 2005. The role of heat shock proteins Hsp70 and Hsp27 in cellular protection ofthe central nervous system. Int J Hyperthermia 21 379-392. 

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