Cataract induction by 1,2-naphthoquinone. II. Mechanism of hydrogenperoxide formation and inhibition by iodide.

Abstract

Naphthalene cataract is probably due to peroxide production through naphthoquinone (NQ) redox cycling and/or glutathione conjugation. Both mechanisms yield losses of essential SH-groups in cristallins and are thus probably involved in protein modification finally visible as lens opacity. 1,2-Naphthoquinone produces H2O2 in the presence of either ascorbate, glutathione, NADH or--to a lesser extend--by homogenates of lens protein preparations. In the presence of 1,2-naphthoquinone and the above reductive additions, both, oxygen uptake and H2O2 formation can be observed. Reductive oxygen activation in these systems are diminuated by iodide in a concentration-dependent manner. Since maleimide-treated proteins are less capable to activate oxygen by 1,2-naphthoquinone, a direct oxygen activation by the interactions of 1,2-naphthoquinone with protein-SH is indicated. Catalysis of "diaphorase"-type (dia) enzymes via NADH--dia--1,2-NQ--O2 seems not to operate in hydrogenperoxide production during 1,2-naphthoquinone lens toxicity.

• Authors: R Kröner, E Kleber, E F Elstner
• Journal: Zeitschrift fur Naturforschung. C, Journal of biosciences (Z Naturforsch C J Biosci) 1991 Mar-Apr Vol. 46 Issue 3-4 Pg. 285-90 ISSN: 0939-5075 [Print] Germany
• PMID: 1878112 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Crystallins
• Iodides
• Naphthoquinones
• 1,2-naphthoquinone
• Hydrogen Peroxide

Topics

• Animals
• Cataract (chemically induced)
• Cattle
• Crystallins (metabolism)
• Hydrogen Peroxide (metabolism)
• Iodides (pharmacology)
• Kinetics
• Naphthoquinones (pharmacology)
• Oxygen Consumption (drug effects)