Acute phase pulmonary response to silica in rats.
DiMatteo-M; Antonini-JM; Van Dyke-K; Reasor-MJ
Toxicologist 1994 Mar; 14(1):90
Silica has been shown to cause inflammation and damage to lung tissue. Study objectives were to determine the minimum time after silica exposure that the inflammatory/damage response was detectable and the temporal relationship of these processes. Male Fischer 344 rats were dosed intratracheally with silica [2.5mg (low) or 10mg (high) /100g body weight] or saline vehicle. At 2 and 4 hrs, post-exposure, both cellular and biochemical parameters of inflammation/damage were evaluated via bronchoalveolar lavage. At 2 hrs, total protein was elevated at both doses (p less than or equal to 0.05), but other parameters were quite variable. By 4 hrs, post-silica exposure all parameters were elevated over the saline control (p less than or equal to 0.05) ith the exception of lDH activity. In a further attempt to describe the inflammatory/damage processes, luminol-dependent chemiluminescence (Cl) was performed on chopped lung. At 4 hrs. post- silica, there was a 5-fold (low dose).and 10-fold (high dose) incre e in stimulated Cl, respectively, over saline control. The addition of inhibitors, superoxide dismutase or N-nitro-l-arginine methyl ester, caused decreases in Cl activity of both dosage groups at both time points (p less than or equal to 0.05). Reductions in Cl activity infer that oxidants playa role in the acute phase response. Study results indicate the initial stages of inflammation/damage begin to appear by 2 hours after silica exposure, but are definitive by 4 hours.
Laboratory-animals; Animal-studies; Quartz-dust; Silica-dusts; Dust-particles; Dust-exposure; Particulate-dust; Airborne-particles; Fibrosis; Pulmonary-system-disorders; Respiratory-system-disorders; Respirable-dust
The Toxicologist. Society of Toxicology 33rd Annual Meeting, March 13-17, 1994, Dallas, Texas
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