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Two groups of 75 rats were injected intraperitoneally with one single dose of 9 mg/kg DMNA and 120 mg/kg DENA, respectively, 28 h after partial hepatectomy. Control groups of non-hepatectomized rats received one single injection of DMNA or DENA at doses of 20 mg/kg and 200 mg/kg, respectively, which were found to be equitoxic to the doses administered to partially hepatectomized rats. One control group of partially hepatectomized rats was injected with saline. Tumors developed in the partially hepatectomized rats injected with nitrosamines with the following frequency: for DMNA: 13% in the liver, 13% in kidney, 4% in lung, 4% at the surgical scar, 9% in hematopoietic tissue and 13% in other organs; for DENA: 11% in liver, 27% in the kidney, 2% at the surgical scar, 2% in hematopoietic tissue, and 11% in other organs. The histological characteristics of these tumors are described. Statistical analysis of the results shows that no significant difference exists in the overall tumor incidence induced by DMNA and DENA and that the difference between liver and kidney tumors induced by DENA is significant, whereas the difference between DMNA- and DENA-induced kidney tumors is less significant. When analyzed by t-test, our results show that death from tumors occurred at an earlier time after DENA than after DMNA treatment and that liver tumors appeared at a significantly earlier time after DENA than after DMNA treatment. Tumors appearing in the same experimental group display similar mean induction times. The possible correlation between metabolic half-life of each nitrosamine in the body and their respective carcinogenic power is discussed. The longer half-life of DENA may be responsible for the shorter tumor induction time observed for this drug, compared to DMNA. The liver tumor incidence, on the other hand, seems to be independent of the half-life but strongly determined by the fact that the proximate carcinogen reaches the hepatic cell during the DNA synthesis phase. [ABSTRACT FROM AUTHOR]

Quercetin is an effective inhibitor of human myeloperoxidase (MPO) activity, both with purified enzyme (IC=3.5 μM) and in a system using stimulated human neutrophils. Quercetin is significantly more potent than three other related compounds (rutin, rutin sulfate and troxerutin) and than methimazole, a previously-known myeloperoxidase inhibitor. The inhibitory activity of quercetin is of the competitive type. Moreover, quercetin is directly able to scavenge hypochlorous acid (HOCl), a chlorinated species generated by the, MPO/HO/Cl system. [ABSTRACT FROM AUTHOR]

Plasma thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured in 84 patients at risk of developing adult respiratory distress syndrome (ARDS) (44 patients following multiple trauma, 29 patients following abdominal surgery and 11 patients with acute pancreatitis). Forty-nine of these 84 patients developed an ARDS. High (greater than 140 pg/ml plasma) TXB2 values were found in 52/84 patients. The median values of TXB2 were: 360 pg/ml in multiple injured, 250 pg/ml in abdominal surgery and 410 pg/ml in acute pancreatitis patients. The median TXB2 value was 575 pg/ml in patients developing ARDS and 140 pg/ml in those without this complication: this difference was statistically significant (p less than 0.05). The median values of 6-keto-PGF1 alpha were 55 pg/ml in multiple injured, 25 pg/ml in abdominal surgery and 120 pg/ml in acute pancreatitis patients. The median 6-keto-PGF1 alpha value was 122 pg/ml in ARDS patients and 25 pg/ml in non-ARDS patients (statistically significant: p less than 0.05). High TXB2 and 6-keto-PGF1 alpha values were particularly related to sepsis in abdominal surgery patients (p less than 0.05) and in multiple injured patients (p less than 0.01). No relation could be established between abnormal TXB2 or 6-keto-PGF1 alpha values and death. High TXB2 values often persisted for several days and were observed particularly at the time ARDS diagnostic criteria were fulfilled.(ABSTRACT TRUNCATED AT 250 WORDS) [ABSTRACT FROM AUTHOR]

The kinetics of incorporation of labelled precursors into the DNA of isolated rat liver mitochondria has been studied after X-irradiation in vitro. Incorporation ofH-TTP was slightly inhibited during the initial period, followed by an increase of about 25 % of the specific activity. Incorporations ofH-TdR andH-BUdR were also stimulated by irradiation of mitochondria, although the amount of incorporated precursor was lower than that ofH-TTP. This radiation-induced incorporation of precursors was abolished by the addition of ethidium bromide or EDTA. Degradation of mt-DNA, indicated by the decrease of specific radioactivity, was observed after irradiation of pre-labelled mitochondria; in presence of EDTA the degradation was not detected. These results were discussed from the viewpoint of the repair synthesis of mitochondrial DNA. [ABSTRACT FROM AUTHOR]

Incorporation of thymidine into nuclear and mitochondrial DNA has been measured in the livers of normal rats and of rats killed 17 h or 24 h after partial hepatectomy. When total-body X-irradiation (500 or 1,500 R) is given at increasing intervals (up to 30 h) before sacrifice, a progressive decrease followed by a plateau of low level of incorporation is observed in the nuclear DNA (N-DNA) whereas the synthesis of mitochondrial DNA (M-DNA) first decreases until a minimal value is reached after 4 h in normal liver and 12 h in regenerating liver, then recovers at an exponential rate, quite independently of the nuclear DNA synthesis. The results suggest that irradiation can interfere with the enzymatic processes of both M-DNA and N-DNA syntheses, but that the persistence of the inhibition of N-DNA synthesis must be ascribed to a temporary block in the cell cycle. The SH-protector AET injected to non-irradiated rats exerts a very small inhibitory effect on normal liver N-DNA and M-DNA synthesis. In regenerating liver, both syntheses are affected rather similarly suggesting a common mechanism of inhibition through impairment of some step in the synthetic process. [ABSTRACT FROM AUTHOR]

Evaluation of lipoperoxidation is performed by 2 methods, the first one measuring the amount of peroxyfunction (−OOH) at a given time, and the second one measuring the accumulation of a degradation product against time. The combination of the 2 methods allows us to investigate the kinetics of lipoperoxidation and to demonstrate, for example, the accelerating effect of lidocaine on autoxidation processes. [ABSTRACT FROM AUTHOR]

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