U. Cornelli - Neuroscience and Aging Institute - Loyola University Chicago

Oxidative stress may be considered as a temporary condition in "normal" subjects if it is tied to an acceleration in energy supplies in relation to demands. Therefore, U.CARR levels in healthy subjects should be lower in persons in a relaxed state than in active persons. This can be seen during the day where levels do increase due to movement, although values still remain within normal ranges (see later on). However, if this involves great muscular activity or particular stress conditions, values may momentary exceed 350 U.CARR but this is to be considered as normal (for example after excercising with a cyclergometer). Values over 350 U.CARR which persist may not, however, be explained by physiological factors whatever the reason. In this case the antioxidant system or reserves are poor or at risk. Some habits such as smoking, also increase free radical levels; experiments have shown that ca 70% of smokers (approx. 20 cigarettes per day) have U. CARR levels between 350-480 U.CARR (see table 1). In these cases the use of particular antioxidants (ARD types or balanced and complete forms) are capable of reducing oxidative levels and hence highlight the relative possibility of reversing oxidative states. The use of contraception causes high increases in levels which arrive at around 400 U.CARR (see table 1) and these levels are not apparently completely reduced by the use of antioxidants. Table 1 d-ROMs values in U.CARR in different conditions and habits CASE CASE NUMBER AVERAGE VALUES ± SD* SMOKING 10 405 ± 62.2 CONTRACEPTION 28 440 ± 34.0 CYCLERGOMETER 10 > 350** * Standard Deviation ** Data refers to values measured immediately after muscular activity; none of the subjects had levels lower than 350 U.CARR. Concerning pathological diseases, attention was paid to chronic inflammatory processes and speckled endothelium pathologies. The reasons for choosing the study of inflammatory diseases is because increases in RD levels were caused by macrophagus prostagladin inflammation. Hence these are pathologies with high free radical productions. Speckled endothelium disease was studied because the endothelium is attacked twice by OH. radicals. As already mentioned, the oxidation of the antiprotease allows much freedom of the protease and these tend to attack  endothelium intercellular joints which open the path to oxidized lipides and other radicals; this renders it easier for macrophagus to penetrate the subendothelium leading to the formation of a lipidic stria which is the initiation of atherosclerosis processes. A number of pathologies may be seen in table 2 and all, except for rheumarthritis, were clinically observed before undergoing specific treatment; all haematic samples were taken in the morning after fasting. From table 2 it may be concluded that average U.CARR levels for the studied pathologies are notably above normal levels, with the exclusion of a few cases of diabetes (non-insulin dependant). All the single cases analyzed had values above the max limit at 300 U.CARR; this reveals that patients are undergoing oxidative stress. Table 2 d-ROMs values in U.CARR for pathological conditions PATHOLOGY CASE NUMBER AVERAGE VALUES ± SD* PSEUDORHEUMATISM 24 451 ± 39 HYPERTRIGLYCERIDEAMIA 11 374 ± 36 NID DIABETES 22 344 ± 30 CAROTID CONSTRICTION 12 374 ± 35 ARTERIAL HYPERTENSION 10 389 ± 33 RAYNAUD'S DISEASE 6 446 ± 29 * Standard Deviation The patients of the pathologies found in table 2 were administered treatment normally used for that particular pathology and once satisfactory results were obtained, U.CARR levels were measured once again in order to evaluate whether oxidation states were modified. The results are found in table 3. Table 3 U.CARR values before and after treatment PATHOLOGY CASE NUMBER AVERAGE VALUES BEFORE AFTER HYPERTRIGLYCERIDEAMIA 11 374 ± 36 332 ± 23* NID DIABETES 22 344 ± 30 355 ± 28 CAROTID CONSTRICTION 12 402 ± 35 378 ± 23 ARTERIAL HYPERTENSION 10 389 ± 33 349 ± 41* RAYNAUD'S DISEASE 6 446 ± 29 422 ± 41 * P < 0.05 test T by Student It was seen that treatment using hypolipaemic and antihypertensive drugs significantly reduced oxidation levels but did not lower values to normal ranges. In a few cases, within various groups, treatment did lead to a compensation in oxidation levels, although this was not so for the majority of cases. It may, therefore, be concluded that oxidation states should be considered as an independent factor. The question remains whether oxidation states should be controlled via the diet or via the use of antioxidant supplements. In conclusion, it is apparent that oxidative stress is an independent risk factor and therefore worsens a number of pathological conditions; the control of oxidant states via the diet or the use of antioxidants may improve pathological conditions on patients with persistently high levels.