nitrogen-dioxide and thiobarbituric-acid

Generation of thiobarbituric acid-reactive substances (TBARS) from methyl linoleate in the exposure of nitrogen dioxide/air was inhibited by beta-carotene in a dose-dependent manner. However, introduction of nitrogen dioxide/air or oxygen into a solution of beta-carotene generated a significant amount of TBARS accompanying loss of its characteristic yellow color. Storing beta-carotene in a solid state at ambient temperatures in air generated a large amount of TBARS accompanying loss of its yellow color. TBARS from beta-carotene may interfere the measurement of TBARS from polyunsaturated fatty acids, and may give undesirable effects on biomaterials.

Topics: Air; beta Carotene; Fatty Acids, Unsaturated; Nitrogen Dioxide; Thiobarbiturates; Thiobarbituric Acid Reactive Substances

Peroxynitrite is the product of the reaction between nitric oxide and superoxide. It is an oxidant which can also decompose to form the hydroxyl radical and nitrogen dioxide. In this report we show that a powerful oxidant with reactivity similar to that of the hydroxyl radical is formed from the generation of superoxide from xanthine oxidase and nitric oxide from S-nitroso-n-acetylpenicillamine (SNAP). Simultaneous generation of these two radicals by either xanthine oxidase/SNAP or the sydnonimine SIN-1 in the presence of low-density lipoprotein (LDL) results in the depletion of alpha-tocopherol and formation of its oxidised product alpha-tocopheroquinone. The mechanism of oxidation required both the formation of nitric oxide and superoxide. In contrast to the promotion of LDL oxidation by transition metals the oxidation of LDL by SIN-1 was not sensitive to the addition of exogenous lipid hydroperoxide.

Topics: Acetaldehyde; Catalase; Free Radicals; Humans; Hydroxides; Hydroxyl Radical; Lipoproteins, LDL; Molsidomine; Nitric Oxide; Nitrogen Dioxide; Oxidation-Reduction; Penicillamine; S-Nitroso-N-Acetylpenicillamine; Superoxide Dismutase; Superoxides; Thiobarbiturates; Vitamin E; Xanthine Oxidase

Lipid peroxide production, antioxidant contents and activities of antioxidative protective enzymes were examined in lungs of rats exposed to clean air (control group), 0.05 ppm O3, 0.05 ppm O3 + 0.04 ppm NO2 and 0.05 ppm O3 + 0.4 ppm NO2 for 22 months. The results were compared with our previous data in rats exposed to 0.04 ppm NO2, 0.4 ppm NO2 and 4 ppm NO2 for their life span (Sagai et al., Toxicol. Appl. Pharmacol., 73, (1984) 444-456). TBA values used as an index of lipid peroxidation in the lungs were increased maximally at 9 months, but were decreased below control values in animals exposed for 18 and 22 months. Nonprotein sulfhydryl (NPSH) contents were increased maximally at 9 months, and after 18 and 22 months were decreased significantly below control values. Vitamin E (VE) contents showed a similar trend. On the other hand, enzyme activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione peroxidase measured by using cumene hydroperoxide (cum.OOH) substrate (GPx-cum.OOH), glutathione peroxidase measured by using H2O2 as a substrate (GPx-H2O2), glutathione S-transferase (GSH-Tase) and superoxide dismutase (SOD) did not show any significant changes during this experiment. The results show that lipid peroxidation in lungs was increased synergistically by a combination of NO2 and O3 at ambient levels, and that the time of maximum lipid peroxide production was shorter than with NO2 alone. The protective ability against lipid peroxides was higher with increased lipid peroxide levels, but the inducibility was not maintained through a life span exposure to the combined gases. Additionally, two small adenomas were observed in 2 out of 18 rats in the 0.05 ppm O3 + 0.04 ppm NO2 group and a large adenoma was observed in 1 out of 18 animals in the 0.05 ppm + 0.4 ppm NO2 group exposed for 22 months.

Topics: Adenoma; Administration, Inhalation; Animals; Atmosphere Exposure Chambers; Breath Tests; Dose-Response Relationship, Drug; Drug Interactions; Lipid Peroxidation; Lung; Lung Neoplasms; Male; Nitrogen Dioxide; Organ Size; Ozone; Rats; Rats, Inbred Strains; Thiobarbiturates

In the current study, biochemical measures of lipid peroxidation following 4-h inhalation exposure to 76 mg/m3 (40 ppm) nitrogen dioxide were correlated with measures of deposition and tissue antioxidant levels in the nasal cavity and the trachea of the Fischer rat. In addition, respiratory-tract mucus samples were collected via esophageal cannulation and nasopharyngeal lavage over known time periods, and were analyzed for phospholipid (PL) content to provide an index of the unsaturated lipids (UL) that they may contain. UL are thought to be important in the scavenging of oxidants by the mucous lining layer. Nasal deposition efficiency, as measured in the surgically isolated upper respiratory tract under unidirectional flow conditions, averaged 25%, corresponding to an absolute deposition rate of 41 nmol/min. Vitamin E levels averaged 1.7, 5.9, and 0.7 nmol/mumol PL in nasal, tracheal, and pulmonary tissues, respectively. The level in the trachea was significantly (p less than 0.005) higher than in the other tissues. As estimated from the increase in lavage PL content over 1 h, the overall mucous PL transport rate was less than 0.013 nmol/min, suggesting the PL of the mucous lining layer could not offer significant protection against the inhaled NO2. Conjugated dienes were detected in two of four pooled nasal tissue samples. Thiobarbituric acid-reactive material levels in tracheal tissues were significantly elevated over control levels by NO2 (p less than 0.05). Thus, despite the relatively high vitamin E levels, 4-h NO2 exposure appeared to result in lipid peroxidation in the trachea and, perhaps, in the nasal airways of the rat, a result that correlated with the apparent lack of oxidant-scavenging species in the mucus lining these airways.

Topics: Animals; Lipid Peroxides; Mucus; Nasal Mucosa; Nitrogen Dioxide; Phospholipids; Rats; Rats, Inbred F344; Respiratory System; Spectrophotometry, Ultraviolet; Thiobarbiturates; Trachea; Vitamin E

This work was done to clarify the relation between the change of lipid peroxidation and the protective systems in lungs after NO2 exposures. JCL:Wistar 8-wk-old male rats were exposed continuously to 10 ppm NO2 for 2 wk. Lipid peroxidation, measured by ethane exhalation in the breath of the rats and by the reaction of thiobarbituric acid with lung homogenates, increased to a maximum at 3 d after a decline at 1 d, and then returned to the initial level (of d 0). Activities of glutathione peroxidase (GPx), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), disulfide reductase (DSR), and superoxide dismutase (SOD) in the 105,000 X g supernatant of lung homogenates were depressed slightly at 1 d. Thereafter, they increased significantly to their maximum levels from 5 to 10 d, and these maximum levels were maintained until d 14. The pattern of change of these protective enzymes was symmetric to that of lipid peroxidation after 3 d. The order of the ratio of the increased value to the initial value was G6PD greater than DSR greater than 6PGD greater than GR greater than GPx greater than SOD. The time course of nonprotein sulfhydryls was similar to that of the protective enzymes. In contrast, the amounts of vitamin E increased to a maximum at 2 d and then returned to the initial level. The periodic change of vitamin E was similar to that of lipid peroxidation rather than that of the protective enzymes. These results suggest that the ability of the enzyme systems in lungs to protect against NO2 fluctuated in a complex manner and the activities of the protective enzymes varied inversely with lipid peroxidation.

Topics: Animals; Ethane; Glutathione Peroxidase; Glutathione Reductase; Glutathione Transferase; Lipid Peroxides; Lung; Male; Nitrogen Dioxide; Rats; Rats, Inbred Strains; Superoxide Dismutase; Thiobarbiturates; Time Factors