Biochemical aspects of cellular antioxidant systems

Aerobic life is characterized by a steady generation of reactive oxygen species balanced by a similar rate of their consumption by antioxidants. To maintain homeostasis, there is a requirement for the continuous regeneration of antioxidant capacity, and if this is not met, oxidative stress occurs, resulting in pathophysiological events. Cellular protection against oxidative stress is organized at multiple levels. Defense strategies include prevention, interception, replacement, and repair. These mechanisms are coupled to the intermediary metabolism for a continuous supply of energy, reducing equivalents, and precursors, and depend on the dietary supply of metabolic fuels and essential molecules to allow an optimal cellular functioning

Influence of industrial pollutants on thyroid function in Channa punctatus (Bloch).

A 30 day exposure of C. punctatus to sublethal levels of phenol, ammonia, mercuric chloride, cadmium chloride and a mixture of the four resulted in an overall activation of guaiacol peroxidase and depression of iodide peroxidase (IPOD) activity and blood T4 titre. Interestingly enough, in case of 15 day ammonia and 1 day mercury exposures, an increase of IPOD activity was accompanied by a decrease in T4 titre. In general, phenol, mercury, cadmium and the mixture of pollutants were found to inhibit LP activity by 56% to 85% while ammonia inhibited lysosomal protease (LP) activity by 70%. Alterations in acid phosphatase (AP) activity indicate changes in the lysosomal membrane characteristics caused by these toxicants. Considering the concomitant alterations in IPOD, T4, LP and AP it is surmised that thyroid function in C. punctatus is influenced by the pollutants by two pathways, one via IPOD pathway affecting T4 synthesis and the other via lysosomal pathway affecting T4 release.