Thiobarbituric acid reactants

There is very little data on ROM production in haemochromatosis in humans. Increases in thiobarbituric acid reactants in plasma were associated with increases in non-transferrin-bound free iron. However, other indices of lipid peroxidation were no different from controls (Peters eta/., 1985). There are no studies of in vivo lipid peroxidation in humans. It is also of interest that levels of antioxidant defences in liver biopsies from patients with haemochromatosis are normal (Selden et /., 1980). 

The concentration of ozone taken up by the media containing linolenic acid is plotted against time after addition in Figure 8. The rate of ozone breakdown is constant (ozone uptake linear with time) for the first two min until about 0.12 ml ozone are absorbed and then the rate decreases sharply, reaching a steady-state rate of ozone uptake between 10-12 min. This first break in the curve corresponds to an ozone uptake of 0.12 ml + (24 moles/liter) = 0.005 millimoles (or 10 M). This is equivalent to 1 mole of linolenic acid added per mole ozone absorbed. Thiobarbituric acid reactant production is also plotted on the same axis. This compound (TBA reactant) probably arises by formation of a three-carbon fragment (malondialdehyde) from the ozone-induced oxidation of linolenic acid (23). The rate of TBA reactant formation is also linear for the first 2 min at which point the curve undergoes a less pronounced break. Malondialdehyde formation ceases immediately when the ozone is shut off (Scrub 1 on). An oxygen control sample produced no malondialdehyde. 

Figure 8. The kinetics of O, uptake ar Thiobarbituric acid reactant produced by ozonolysis of linolenic acid. From the Os uptake described in Figure 7, the amount of Os is calculated by integrating the area under the - -l-linolenic curve (in ppm/min) and multiplying by the air flow rate (ml/min). The Thiobarbituric acid (TEA) reactant assayed according to Heath b- Packer (23), is given as absorbance difference (A 532-A 580).

Figure 10. Production of malondialdehyde, the change in Chlorella viability and uptake of O3 by a suspension of Chlorella cells. A sample from a culture of 38°C grown C. sorokiniana uflr. pacificensis (3 X10 cells/ml autotrophic medium) was treated with 180 ppm ozone. Thiobarbituric acid reactants were assayed by the method of Heath b- Packer (23), viable cells by plating on glucose-supplemented agar medium, and ozone uptake on a Cary spectrophotometer as described in Figures 6-8.

In our attempts to determine the possible role of free radical lipid peroxidation in smoke induced injury, the levels of lipid peroxidation products - thiobarbituric acid reactants, mainly malondialdehyde - wereQmeasured in lung homogenates with or without prior incubation at 37 C for one hour, contrary to our expectation, the levels of thiobarbituric acid reactants were found to be decreased, rather than increased, in the lungs of cigarette-smoke-exposed rats (Table III). Such a depression effect, however, was observed only when animals were exposed to whole smoke, and not to the gaseous phase of smoke. 

Table III. Dietary Vitamin E and Thiobarbituric Acid Reactants in the Lungs of Cigarette-Smoked Rats ...

Isolated hepatocytes incubated with ionic iron rapidly undergo lipid peroxidation. Some studies have not shown a consequent decrease in viability (as indicated by uptake of trypan blue or release of enzymes). This is probably a result of short incubation times, as changes in viability lag behind increases in lipid peroxidation, and may not occur for more than 2 h after lipid peroxidation begins (Bacon and Britton, 1990). Recent studies have shown strong correlations between increased lipid peroxidation [production of thiobarbituric acid (TBA) reactants] and loss of cell viability (trypan blue staining) (Bacon and Britton, 1989). The significance of the lag between lipid peroxidation and decreases in cell viability is as yet uncertain. 

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