BIOCHEMICAL MARKERS OF DAMAGE IN RATS EXPOSED BY ORAL GAVAGE TO SINGLE-WALLED CARBON NANOTUBES IN COMBINATION WITH ANTIOXIDANT PREPARATION “AEVIT”

Introduction. The toxicity of carbon nanotubes (CNT), which are chemically inert particles, is thought to be connected with responses of aseptic inflammation and oxidative stress. This study was conducted to determine how far antioxidants may reduce CNT toxicity in laboratory animals. Material and methods. Male Wistar rats were administered by oral gavage with 0.05 or 0.5 mg/kg/day of Tuball© single-walled CNT in vegetable oil for 2 weeks, without a modifier or in combination with Aevit© (mixture of retinol and α-tocopherol given in doses 25,000 IU/kg/day and 25 mg/kg/day correspondingly). Control animals received oil or Aevit without CNT. 10 markers of oxidative stress and 12 clinical chemistry markers were determined in the rat blood samples. Results. Aevit didn’t influence the above biochemical markers, but combination “Aevit + CNT” increased the prooxidant action of CNT and arose biochemical signs of malabsorption, presumably as a result of retinol inhibitory action onto repair of intestinal epithelial cells, damaged by CNT. Discussion. The lack of tocopherol protective action, which usually removes prooxidant effects of high retinol concentrations, can be explained by superposition of two mechanisms: 1) two components of Aevit, in the presence of CNT, may be separated in space, since only retinol has isoprenoid side chain needed for the formation of donor-acceptor complexes with CNT surface; 2) the effects of retinol on cell reproduction, differentiation and wound healing is not related to its anti - or pro-oxidant properties but takes place at the level of target genes transcription after binding of retinoic acid with nuclear receptors RARs and RXRs. The data obtained allowed supposing the mechanism of lung cancer increases in ATBC and CARET trials was not prooxidant action of retinol and its precursor β-carotene, but regulatory inhibition of lung epitheliocytes reparation during its continued damage by cigarette smoke and asbestos fibers by retinoic acid. Conclusion. Aevit (and, probably, other retinoid-containing preparations) can’t be recommended to ensure the safety of humans and animals during oral CNT intake. The results obtained explanation needs both functional activities of retinol, which is simultaneously antioxidant and one of the nuclear regulators; this, in turn, leads to the new assumption about the mechanisms of unsuccessful outcomes in ATBC and CARET trials.

Quality, Microstructure, and Technological Properties ofSheepMeat Marinated in Three Different Ways

The objective of this study was to explore the effect of 24 and 48 h alkaline (2% pentasodium tripolyphosphate), acid (2% sodium lactate), and water-oil marinating (water : sun flavor oil = 1 : 1 and 2% salt) as well as brine soaking (2% salt) on microstructure, changes in protein, and lipid fractions and technological properties of sheep (m. Longissimus dorsi). Strong myofibrillar fragmentation after 48 h alkaline marinating was observed. Significant swelling and increasing of spaces between myofibrils were found after 24 h brine soaking. Marinating in water-oil emulsions did not show a significant impact on the muscle microstructure. Alkaline and acid marinating as well as salt soaking promote the myofibrillar protein solubility and increased the free amino nitrogen content. After 24 h acid and 48 h alkaline marinating SDS-PAGE electrophoresis showed increasing of 25–30 kDa protein bands. The results obtained for the lipid and protein oxidation confirm prooxidant action of the sodium lactate (2%) and antioxidant effect of polyphosphates (2%) in marinated sheep.

Antioxidant vs. prooxidant action of phenothiazine in a biological environment in the presence of hydroxyl and hydroperoxyl radicals: a quantum chemistry study

In aqueous solution, phenothiazine regenerates and acts as an excellent antioxidant while in lipid media, it behaves as a prooxidant.

Bixin and Norbixin Have Opposite Effects on Glycemia, Lipidemia, and Oxidative Stress in Streptozotocin-Induced Diabetic Rats

The present study investigated the effects of oral administration of annatto carotenoids (bixin (BIX) and norbixin (NBIX)) on glucose levels, lipid profiles, and oxidative stress parameters in streptozotocin (STZ)-induced diabetic rats. Animals were treated for 30 days in the following groups: nondiabetic control, diabetic vehicle, diabetic 10 mg/kg BIX, diabetic 100 mg/kg BIX, diabetic 10 mg/kg NBIX, diabetic 100 mg/kg NBIX, diabetic metformin, and diabetic insulin. Blood glucose, LDL cholesterol, and triglyceride levels were reduced in the diabetic rats treated with BIX. BIX treatment prevented protein oxidation and nitric oxide production and restored superoxide dismutase activity. NBIX treatment did not change most parameters assessed, and at the highest dose, it increased LDL cholesterol and triglycerides levels and showed prooxidant action (increased protein oxidation and nitric oxide levels). These findings suggested that BIX could have an antihyperglycemic effect, improve lipid profiles, and protect against damage induced by oxidative stress in the diabetic state. Because NBIX is a water-soluble analog of BIX, we propose that lipophilicity is crucial for the protective effect of annatto carotenoids against streptozotocin-induced diabetes.

Antioxidant/Prooxidant and Antibacterial/Probacterial Effects of a Grape Seed Extract in Complex with Lipoxygenase

In an attempt to determine the antioxidant/prooxidant, antibacterial/probacterial action of flavan-3-ols and procyanidins from grape seeds, pure catechin (CS), and an aqueous grape seed extract (PE), were applied in the absence and presence of pure lipoxygenase (LS) or in extract (LE) to leucocyte culture,Escherichia coli B41andBrevibacterium linens, and observed whether there was any effect on lipid peroxidation, cytotoxicity, or growth rate. Short time periods of coincubation of cells with the polyphenols, followed by the exposure to LS and LE, revealed a high level of lipid peroxidation and a prooxidative effect. Longer coincubation and addition of LS and LE resulted in the reversal of the prooxidant action either to antioxidant activity for CS + LS and PE + LS or to the control level for CS + LE and PE + LE. Lipid peroxidation was significantly reduced when cells were exposed to polyphenols over a longer period. Longer exposure ofE. colito CS or PE followed by addition of LS for 3 h resulted in bactericidal activity. Significant stimulatory effect on microbial growth was observed for PE + LS and PE + LE treatments inB. linens, illustrating the potential probacterial activity inB. linenscultures. Lipoxygenase-polyphenols complex formation was found to be responsible for the observed effects.

Correlation between mammalian cell cytotoxicity of flavonoids and the redox potential of phenoxyl radical/phenol couple.

Flavonoids exhibit prooxidant cytotoxicity in mammalian cells due to the formation of free radicals and oxidation products possessing quinone or quinomethide structure. However, it is unclear how the cytotoxicity of flavonoids depends on the ease of their single-electron oxidation in aqueous medium, i.e., the redox potential of the phenoxyl radical/phenol couple. We verified the previously calculated redox potentials for several flavonoids according to their rates of reduction of cytochrome c and ferricyanide, and proposed experimentally-based values of redox potentials for myricetin, fisetin, morin, kaempferol, galangin, and naringenin. We found that the cytotoxicity of flavonoids (n=10) in bovine leukemia virus-transformed lamb kidney fibroblasts (line FLK) and murine hepatoma (line MH-22a) increases with a decrease in their redox potential of the phenoxyl radical/phenol couple and an increase in their lipophilicity. Their cytotoxicity was decreased by antioxidants and inhibitors of cytochromes P-450, α-naphthoflavone and isoniazide, and increased by an inhibitor of catechol-O-methyltransferase, 3,5-dinitrocatechol. It shows that although the prooxidant action of flavonoids may be the main factor in their cytotoxicity, the hydroxylation and oxidative demethylation by cytochromes P-450 and O-methylation by catechol-O-methyltransferase can significantly modulate the cytotoxicity of the parent compounds.