Effects of co-supplementation of iron with ascorbic acid on antioxidant--pro-oxidant balance in the guinea pig.

The relationship between intake of iron with ascorbic acid and their uptake into the plasma and liver of guinea pigs was studied. The influence on the antioxidant/pro-oxidant balance of liver microsomes was also determined. Animals were fed a standard pelleted diet low in iron and ascorbic acid for 35 days.

Investigation of the role of reactive oxygen species in bilirubin metabolism in the Gunn rat.

It has been previously established that the attenuation of hepatic lipid peroxidation by a fat-free diet is accompanied by a marked rise in plasma bilirubin in Gunn rats. Present in vitro studies confirmed that microsomal lipid peroxidation caused the concurrent degradation of added bilirubin but failed to show that microsomal superoxide, hydroxyl radical or hydrogen peroxide would degrade bilirubin. Moreover, although injection of vitamin E completely inhibited microsomal lipid peroxidation and bilirubin degradation it had no effect on plasma bilirubin.

Antioxidants impair the coupling of cell-surface ligand receptors to the inositol lipid signalling pathway in human T lymphocytes but not in Jurkat T lymphoblastic leukemia cells. Evidence that leukotrienes are not involved in the coupling mechanism.

Ligands including phytohaemagglutinin (PHA) and anti-CD3 monoclonal antibodies trigger the generation of inositol lipid-derived second messengers following their binding to cell-surface structures of human T lymphoid cells. Previous evidence has suggested that the generation of leukotrienes may play an intermediary role in coupling the ligation of T lymphoid cell-surface structures to the inositol lipid signalling system in these cells (A.R.

Lipid peroxidation in electroporated hepatocytes occurs much more readily than does hydroxyl-radical formation.

1. Rat hepatocytes suspended in 0.25 M-sucrose were electropermeabilized.

Dietary modulation of plasma bilirubin and of hepatic microsomal lipid peroxidation in the Gunn rat.

An in vitro assay for the simultaneous measurement of lipid peroxidation (LPO) and bilirubin degradation (BRD) activities in rat liver microsomes has been developed; a good correlation between the 2 activities was observed (r = 0.78). In the Gunn rat a lipid free diet caused an increase in plasma bilirubin (62.

An investigation of the transverse topology of bilirubin UDP-glucuronosyltransferase in rat hepatic endoplasmic reticulum.

Bilirubin UDP-glucuronosyltransferase (UDPGT) activity in sealed hepatic microsomes from clofibrate-treated rats was highly latent and was fully expressed by disruption of vesicles with detergents. Antibodies raised against purified bilirubin UDPGT were used to study the transmembrane orientation of the protein to provide a molecular understanding of the UDPGT latency. Immunoblot analysis of sealed microsomes, and microsomes after treatment with proteinases, showed that only a small portion of the protein resides on the cytoplasmic side of the microsomal vesicles.

Iron overload and the predisposition of cells to antioxidant consumption and peroxidative damage.

We have investigated the effects of iron overload in vivo on the tocopherol levels and the extent of lipid peroxidation in rat liver microsomes and their response to subsequent oxidative stress in vitro. The results demonstrate a direct correlation between consumption of antioxidant defences and the induction and extent of malondialdehyde production in microsomes prepared from iron-loaded rats. The data are consistent with the requirement for iron (II)/iron (III) ratios in lipid peroxidation in control microsomes.

Inhibition of the formation of myotubes in vitro by inhibitors of transglutaminase.

The effects of competitive inhibitors of transglutaminase on the formation of myotubes by the fusion of myoblasts in vitro has been investigated. Myotube formation was inhibited when myoblasts from 11-day-old chick embryos were cultured in vitro in the presence of 10 mM histamine or 0.2 mM dansyl cadaverine.

Effects of retinol, fatty acids and glycerol monooleate on the fusion of chick embryo myoblasts in vitro.

Cell fusion of embryonic chick myoblasts has been studied in the presence of fat-soluble agents that induce erythrocytes to fuse. Retinol inhibited myoblast fusion but the cells recovered their ability to fuse within 48 h of removal of the retinol from the medium. Myristic acid, oleic acid, glycerol monooleate, linolenic acid and arachidonic acid similarly prevented fusion in myogenic cultures.

Diazobenzenesulphonate selectively abolishes stimulation of glucuronidation by UDP-N-acetylglucosamine.

1. Basal rates of glucuronidation of oestrone (guinea pig) or of 4-nitrophenol (rat or guinea pig) were not significantly altered in sealed liver microsomal vesicles, treated with the membrane-impermeant protein-modifying agent diazobenzenesulphonate at 0.5-1.

Fabry-Perot-interferometer imaging system for thermospheric temperature and wind measurements.

Doppler-broadened Fabry-Perot fringes of weak (<1-kR) auroral [OI] 5577- and 6300-A emissions have been detected in real time (1/60 sec) with the aid of a low-light level image-orthicon TV camera coupled to a two stage image intensifier. The imaging scheme permits static-mode operation of a Fabry-Perot interferometer. For maximum use of all the information contained in every TV frame, each circular fringe may be sectioned into several annuli, and the corresponding annuli from all rings are summed to yield an intensity value.

Studies on the inhibition of hepatic microsomal glucuronidation by uridine nucleotides or adenosine triphosphate.

The ability of five nucleotides in the presence of excess divalent cations to inhibit UDPglucuronosyltransferase in sealed or leaky liver microsomal vesicles was studied. Two nucleotides inhibited potently while three others were weak inhibitors. At low concentration, both of the potent inhibitors, uridine tri- and diphosphates tended to inhibit more in sealed microsomal vesicles than in leaky microsomes, while the weak inhibitors, uridine diphosphate glucose and adenosine triphosphate behaved in the opposite manner and inhibited less in sealed than in leaky microsomes.

The influence of diet and diabetes on stearoyl Conenzyme A desaturase (EC 1.14.99.5) activity and fatty acid composition in rat tissues.

1. Rats were given low-fat diets for 3 d in which the carbohydrate source was starch. The livers of animals given the fructose or sucrose had increased hepatic activities of the fatty acid synthetase and stearoyl CoA desaturase (EC 1.

Phospholipid content and activity of pure uridine diphosphate-glucuronyltransferase from rat liver.

Rat liver phospholipids were radioactively labeled in vivo before purification of UDP-glucuronyltransferase to homogeneity. The pure enzyme contained very little phospholipid (approx. 0.