The inhalation of
silica has been shown to produce a dramatic inflammatory and toxic response within the lungs of humans and laboratory animals. A variety of cellular and biochemical parameters are used to assess the
silica-induced
lung injury. The purpose of this paper is to introduce the use of
luminol-dependent chemiluminescence as a new method to study
inflammation in both phagocytic cells and lung tissue recovered from
silica-exposed animals. Chemiluminescence, or the emission of light, accompanies the release of reactive forms of
oxygen when phagocytic cells are challenged. In this study, male Fischer 344 rats were intratracheally instilled with either
silica (10 mg/100 g bw) or saline vehicle. One day after the instillations, a marked increase in the chemiluminescence was observed in the lung tissue and bronchoalveolar lavage cells recovered from the
silica-treated animals when compared with the saline controls. The light reaction was markedly decreased by either
superoxide dismutase of N-nitro-
arginine methyl ester hydrochloride.
Superoxide dismutase is involved in the enzymatic breakdown of
superoxide anion, while N-nitro-
L-arginine methyl ester hydrocholoride, a
nitric oxide synthase inhibitor, prevents the formation of
nitric oxide. When
superoxide anion and
nitric oxide react, they form the highly oxidizing substance
peroxynitrite. This study then implicates
peroxynitrite as an agent that may be responsible for some of the
oxidant lung injury that is associated with
silica exposure. The use of
luminol-dependent chemiluminescence may prove valuable as a method to measure the earliest events in the inflammatory process, and may be an adjunct in studying the mechanisms that produce
inflammation.