Tissue protection against oxidative stress

Abstract

We used an enhanced luminescence technique to study the response of rat tissues, such as liver, heart, muscle and blood, to oxidative stress and to determine their antioxidant capacity. As previously found for liver homogenate, the intensity of light emission (E) of tissue homogenates and blood samples, stressed with sodium perborate, is dependent on concentration, and the dose-response curves can be described by the equation E = a.C/exp(b.C). The b value depends on the antioxidant defence capability of the tissues. In fact, it increases when homogenates are supplemented with an antioxidant, and is correlated with tissue antioxidant capacity, evaluated by two previously set up methods both using the same luminescence technique. Our results indicate that the order of antioxidant capacity of the tissues is liver > blood > heart > muscle. The a value depends on the systems catalysing the production of radical species. In fact, it is related to the tissue level of hemoproteins, which are known to act as catalysts in radical production from hydroperoxides. The equation proposed to describe the dose-response relation is simple to handle and permits an immediate connection with the two characteristics of the systems analysed which determine their response to the pro-oxidant treatment. However, the equation which best describes the above relation for all the tissues is the following: E = alpha. C/exp(beta.C delta). The parameter delta assumes values smaller than 1, which seem to depend on relative amounts of tissue hemoproteins and antioxidants. The extension of the analysis to mitochondria shows that they respond to oxidative stress in a way analogous to the tissues, and that the adherence of the dose-response curve to the course predicted from the equation E = a.C/exp(b.C) is again dependent on hemoprotein content.

T3 and the thyroid hormone β-receptor agonist GC-1 differentially affect metabolic capacity and oxidative damage in rat tissues

“…C, control euthyroid rats; H, hypothyroid rats; H+T 3 , hypothyroid T 3 -treated rats; H+GC-1, hypothyroid GC-1-treated rats. Because the level of light emission, and particularly the emission maximum, can be considered an index of the susceptibility of the preparations to oxidative challenge (Di Meo et al, 1996), our results reveal an increased susceptibility following both treatments, but in smaller measure with GC-1.…”

Effect of thyroid state on enzymatic and non-enzymatic processes in H2O2 removal by liver mitochondria of male rats

“…2) was described by the equation [E = a·C/exp(b·C)], in which a and b are two constants. The a value is related to the concentration of substances, such as the cytochromes, able to react with H2O2 to produce HO • radicals inducing the luminescent reaction, whereas the b value is related to the concentration of substances able to prevent the formation or interacting with HO • radicals, thus reducing the levels of light emission (Di Meo et al, 1996;Venditti et al, 1999). Such levels were lower in hypothyroid than in euthyroid preparations (Fig.…”

“…The plates were incubated at 37°C for 30 s under continuous shaking and then transferred to a luminescence analyzer (Amerlite Analyzer). The emission values were fitted to dose-response curves using the statistical facilities of the The determination of the overall antioxidant capacity (CA) was performed according to Di Meo et al (1996). Briefly, 250 μl of RM was added to 10 μl of 110 ng/ml peroxidase plus 15 μl of either desferrioxamine, at concentrations ranging between 0.01 and 3 mM, in 15 mM Tris (pH 8.5) or buffer alone.…”

The ethanolic extract of Kaempferia parviflora reduces ischaemic injury in rat isolated hearts

“…Reactive oxygen species lead to lipid peroxidation and protein oxidation, causing cell death via apoptosis and ROS-mediated myocardial dysfunction (Gross et al, 1999;Penna et al, 2009). Susceptibility to oxidative stress is higher in the heart than in other organs because of low levels of antioxidant enzymes (Di Meo et al, 1996). Therefore, either administration of exogenous antioxidants or upregulation of endogenous antioxidant is an important therapeutic strategy to prevent cardiac ischaemic injury against ROS (Qin et al, 2009;Wattanapitayakul and Bauer, 2001).…”