Disease relevance of NSC4733

• Use of an ion exchange chromatographic method and a colorimetric method with thiobarbituric acid showed that levels of nonenzymatically glucosylated serum albumin were increased in patients with poorly controlled diabetes mellitus compared to controls [1].
• PR-39 also inhibited ischemia and the high K+-mediated increase in lung thiobarbituric acid reactive substance [2].
• Tumor growth in rabbits treated with hyperthermia was significantly reduced, and thiobarbituric acid-reactive substances in the tumor tissue treated with hyperthermia were significantly increased until 6 h after hyperthermia [3].
• Hepatoma cells enriched with this concentration were further incubated to determine their susceptibility to lipid peroxidation; mortality increased in parallel with increased thiobarbituric acid-reactive substance production [4].
• Evaluation of light-induced MKT-077 lipid peroxidation in mitochondrial membrane fragments by the thiobarbituric acid test and by measurement of nonrespiratory-linked oxygen uptake suggests that mitochondrial phototoxicity by MKT-077 may be the result of lipid peroxidation via reactive oxygen species [5].

Psychiatry related information on NSC4733

• Elevated thiobarbituric acid-reactive substances and antioxidant enzyme activity in the brain in Alzheimer's disease [6].
• Effects of aging and dementia on the levels of thiobarbituric-acid-reactive products stimulated by L-glutamic acid in human autopsy and biopsy brain tissue [7].
• The parameters studied were memory acquisition and memory retention, locomotor activity and thiobarbituric acid reactive substances, as an index of lipid peroxidation [8].
• The effect of variables was tested by the Youdens ruggedness test (reaction time, temperature, cooling, concentration of sample, thiobarbituric acid, water, heavy metals, antioxidants, chelating agents, bubbling with oxygen or nitrogen) [9].

High impact information on NSC4733

• Probucol treatment was associated a threefold increase in LDL resistance to copper-induced oxidative modification (P < 0.05) and a reduction in tissue lipid peroxidation (as assessed by thiobarbituric acid-reactive substances; P < 0.05) compared to animals fed cholesterol alone [10].
• Modified LDL, isolated from pooled LDL of 10 patients, showed a higher electrophoretic mobility on agarose gels, a higher content of thiobarbituric acid reactive substances, and a higher cholesterol/protein ratio than native LDL and had a similar reactivity (antigen/protein ratio) in the assay as the in vitro MDA-modified LDL used for calibration [11].
• Both ascorbate and probucol inhibited the oxidative modification of LDL in both systems to a similar degree as evidenced by the thiobarbituric acid-reacting substance activity, electrophoretic mobility, and degradation by macrophages [12].
• Modification of low density lipoproteins by human arterial smooth muscle cells was characterized by increased electrophoretic mobility and increased content of malondialdehyde-like oxidation products reactive with thiobarbituric acid [13].
• Glucosylation of insoluble human tendon collagen, a protein with little or no turnover was determined by a thiobarbituric acid method in 23 subjects as a function of age and the presence or absence of diabetes [14].

Chemical compound and disease context of NSC4733

• Merbarone, a nonsedating derivative of thiobarbituric acid, has demonstrated excellent activity against certain murine tumors, including L1210 and P388 leukemias, B16 melanoma, and M5076 sarcoma [15].
• Plasma lipid peroxides were measured as malonyldialdehyde (MDA) by the thiobarbituric acid (TBA) method in 75 children suffering from Plasmodium falciparum malaria [16].
• The accumulation of the aldehydic lipid peroxidation product 4-hydroxynonenal and thiobarbituric acid-reactive substances was demonstrated during anoxia/reoxygenation of isolated rat hepatocytes [17].
• Glutathione S-transferase increased, whereas superoxide dismutase and thiobarbituric acid reactive substances decreased in melanoma samples in direct relation to the Clark levels [18].
• Incubation of rat liver cell-free extracts with an NADPH-generating system and with nifurtimox or benznidazole (two nitroheterocyclic drugs used in the treatment of Chagas' disease) produced oxidation of reduced glutathione (GSH) and increased lipid peroxidation, as shown by the generation of thiobarbituric-acid-reacting intermediates [19].

Biological context of NSC4733

• CCl4 or 14CCl4 was added to the sealed flask that contained the system, and after 20 min CHCl3 production, thiobarbituric acid-reactive substances (an index of lipid peroxidation), and covalent binding of 14C were measured [20].
• Cytochrome P450 2E1, mitochondrial generation of peroxides, thiobarbituric acid reactants, and ethane exhalation were increased [21].
• Oxidative stress as assessed by the hepatic level of thiobarbituric acid reacting substances, was evident at 10 weeks but more pronounced at 17 weeks [22].
• Under these conditions, the extent of lipid peroxidation was assessed as thiobarbituric acid reactive substances formation and the energy transducing capability of the inner mitochondrial membrane was evaluated by membrane potential measurements [23].
• Tumors were investigated for: (a) thiobarbituric acid-reactive substance formation and protein-bound 4-hydroxynonenal, as indicators of lipid peroxidation; (b) reactive oxygen-mediated protein modifications; (c) apoptosis; and (d) tumor volume growth [24].

Anatomical context of NSC4733

• Thiobarbituric acid reactive substances, a measure of lipid peroxidation, doubled in isolated lysosomal membranes [25].
• Hepatic mitochondria and microsomes (humans only) were isolated, and lipid peroxidation was measured by lipid-conjugated dienes and thiobarbituric acid-reacting substances [26].
• In view of this information, the amount of thiobarbituric acid-reactive substances (lipid peroxidation products) present endogenously in liver and mammary gland was quantitated [27].
• Ascorbic acid (0.2 mM) induced lipid peroxidation in cultured human fibroblasts judging by the production of thiobarbituric acid-reactive substances and carbonyl groups, and by the presence of malondialdehyde- and 4-hydroxynonenal-protein adducts [28].
• Serum levels of thiobarbituric acid reactive substances predict cardiovascular events in patients with stable coronary artery disease: a longitudinal analysis of the PREVENT study [29].

Associations of NSC4733 with other chemical compounds

• As nonspecific indicators of lipid peroxidation, measurements of the loss of unsaturated fatty acid in the phospholipids together with the generation of hydroperoxide breakdown products were done with the use of the thiobarbituric acid test [30].
• No differences were present in total glutathione, thiobarbituric acid reactivity, or superoxide dismutase and glutathione peroxidase activity in the ischemic zones of the two groups [31].
• On the contrary, LDL from group A rabbits incubated with cupric ion showed a 7.4-fold increase in peroxides (thiobarbituric acid-reactive substances) and a 4.3-fold increase in the synthesis of cholesteryl ester in macrophages compared to those of LDL from group B rabbits [32].
• Free radical production was inferred from the relative increase in dichlorofluorescein fluorescence, and the degree of lipid peroxidation was determined by assaying thiobarbituric acid-reactive substances [33].
• Lipid peroxidation as assessed by thiobarbituric acid reacting substance assay was lower in liver homogenate and mitochondrial and microsomal fractions from ethanol-fed pigs than in controls [34].

Gene context of NSC4733

• Mice heterozygous for disruption of the Lias gene develop normally, and their plasma levels of thiobarbituric acid-reactive substances do not differ from those of wild-type mice [35].
• Acetylcholine caused eNOS activation in cells incubated with 10 microgram/ml oxLDL (10-15 thiobarbituric acid-reactive substances) and blocking antibodies to CD36, whereas cells treated with only oxLDL were unresponsive [36].
• The inactivation of TFPI was strongly negatively correlated with both an increase in the net electrical charge of LDL (r = -.80, P < or = .0001) and with the production of thiobarbituric acid-reactive substances (r = -.78, P < or = .0001) and lipid peroxides (r = -.80, P < or = .0001) [37].
• Indices of oxidative stress, including thiobarbituric acid reactive substance, carbonyl protein content, and HO activity, were determined [38].
• Pretreatment with inhibitors of protein kinase C, phospholipase A2 or COX, LOX, COX-2 partially blocked KCN-induced formation of thiobarbituric acid reactive substance, whereas coincubation of L-NAME with the inhibitors decreased lipid peroxidation by 60 to 90% [39].

Analytical, diagnostic and therapeutic context of NSC4733

• We suggest that patients who do not have an explanation for their elevated HbA1c should have GHb measured by the TBA method or affinity chromatography because hemoglobin electrophoresis does not identify this confounding artifact [40].
• We determined plasma levels of fibrinogen (Clauss' method), coagulation factor VII:activity (clotting assay), factor VII antigen, protein C and S antigen, von Willebrand factor antigen, D-dimer concentration (ELISA), and lipid peroxide levels (thiobarbituric acid) in relation to urinary albumin excretion rate (RIA) [41].
• Tissue contents of thiobarbituric acid-reactive substances did not increase during reperfusion in controls, but was reduced in group 4 (p < .004) [42].
• The concentration of substances which react to thiobarbituric acid (TBARS) was measured as a marker of the degree of peroxidation using the HPLC method [43].
• Plasma lipid peroxides were measured in venous blood as the adduct formed between thiobarbituric acid and malondialdehyde (MDA) using high performance liquid chromatography [44].

References