Three model systems measure oxidation/nitration damage caused by peroxynitrite.

Diseases activate the innate immune response which causes ancillary damage to the human body. Peroxynitrite (OONO-) or its carbon dioxide derivatives cause oxidation/nitration and hence mutation to various body polymers e.g. DNA, RNA, protein, lipids and sugars. The control of the ancillary damage can come from antioxidants which inhibit control the amount of peroxynitrite available for damage. In this paper we have developed three different levels of antioxidant screening: (i) Peroxynitrite or SIN-1 reaction with luminol to produce light, and the inhibition of light by substances therefore represents antioxidation. (ii) Nicking of plasmid DNA occurs via oxidants: and is prevented by antioxidants. (iii) Detection of plasmid luciferase activity post-oxidation and infection indicates either prevention or repair of damage: via antioxidants. We found green tea and a number of its polyphenolic constituents effective only at the first level of antioxidation, while extracts of various fruit help at all levels antioxidation. In the final analysis, a combination of green tea extracts and fruits is suggested to produce more complete antioxidant protection.

Galactosamine [GaIN] inhibits luminol-dependent chemiluminescence of human polymorphonuclear leukocytes

The aim of the present study was to examine the effect of D- galactosamine HCl [GaIN] on the oxidative respiratory burst of isolated human polymorphonuclear leukocyte [PMNs]. GaIN added in vitro to PMNs caused a marked inhibitory effect on the luminol- dependent chemiluminescene [CL] induced by phorbol myristate acetate [PMA] on PMNs. The inhibitory effect produced by GaIN was both dose and time dependent when PMA was used to stimulate the oxidative burst of PMNs. The effect of GaIN on the isolated PMNs was partially irreversible, following washing of the GaIN-treated PMNs with phosphate buffered saline [PBS]. PMNs viability was not significantly altered by incubation with GaIN. Addition of lipopolysaccharide [endotoxin] to isolate PMNs in the presence or absence of GaIN did not alter the oxidative burst of PMNs. Addition of oxygen-free radical scavengers enhanced the inhibitory effect induced by GaIN on PMNs CL. In a cell free medium, GaIN has no inhibitory effect on CL induced by luminol, H2O2 and horse radish peroxidase. As a conclusion, results suggested that in vitro, GaIN has a remarkable inhibitory effect on the release of oxygen products from stimulated PMNs