Toxic effects of fatty acid anilides on the oxygen defense systems of guinea pig lungs and erythrocytes

Abstract

Toxic oil syndrome (TOS) is caused by ingestion of denatured edible oils. Even though the etiology and pathogenesis of this disease are not fully known, it is quite clear that generation of free radicals caused by ingestion of fatty acid anilides is responsible for the pathogenetic mechanism in many TOS patients. Fatty acid anilides may also alter the free radical status of lungs and erythrocytes; this possibility may shed some light on understanding toxic oil syndrome. The present study describes the effects of oral administration of fatty acid anilides on the activities of major enzymes involved in the oxygen defense systems of lungs and erythrocytes. Feeding fatty acid anilides caused an increase in the superoxide dismutase (SOD) activity in erythrocytes, whereas it caused a decrease in the SOD activity in lungs. GSH-Px activity was not significantly changed in erythrocytes but was decreased in lungs. Although the activity of catalase was increased only by a higher dose in the erythrocytes, it was not affected in the lung at any dosage. Even though the ingestion of fatty acid anilides caused an increase in the SOD activity in the erythrocytes and a decrease in the SOD activity in the lungs, there was an increase in the lipid peroxidation in both cases. The increase in lipid peroxidation in erythrocytes is probably caused by the accumulation of H2O2, and that in the lungs is due to the accumulation of superoxide anion.

Benzo(a)pyrene‐induced acute neurotoxicity in the F‐344 rat: role of oxidative stress

“…To validate this activity, a SOD assay was performed using cytochrome c as described previously (Mukherjee et al, 1994;Das et al, 1993).…”

“…Malondialdehyde (MDA) levels were determined by the modified method of Ohkawa et al (1979) as described previously Mukherjee et al, 1994). Tissue extract was added to sodium dodecyl sulfate and incubated at room temperature for 10 min.…”

Development of pancellular toxicity in guinea pig lung by ingestion of oleylanilide

“…Thus, the deposition of H202 may be etiologically related to the observed electron dense materials on the surface of the alveolar wall of lungs from OA-treated animals. We have reported earlier that OA ingestion causes a decrease in the activity of superoxide dismutase and glutathione peroxidase and an increased lipid peroxidation in the lung (27). It is known that superoxide radicals can inhibit glutathione peroxidase (28) and that H202 is a potent inhibitor of SOD (29).…”

“…It is known that superoxide radicals can inhibit glutathione peroxidase (28) and that H202 is a potent inhibitor of SOD (29). Therefore, the decrease in the activity of SOD in lung due to OA ingestion (27) may account for the accumulation of superoxide radicals which may lead to lung injury. It has also been reported by Martin et al (10) that anilides cause generation of free radicals in lungs.…”