Toxicity of oleic acid anilide in rats

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Abstract
In the present investigation, we have studied the toxic potential of oleic acid anilide (OAA) and heated oleic acid anilide (HOAA) in relation to the toxic oil syndrome (TOS). Male Sprague-Dawley rats were given 250 mg/kg of OAA or HOAA in mineral oil by gavage, on alternate days for 2 weeks (total 7 doses). The control rats received an equal volume of mineral oil only. The animals were sacrificed at days 1, 7, and 28 following the last dose. Ratio of organ-to-body weight showed increases in spleen and kidney of HOAA and OAA treated rats, respectively, at day 1 while this ratio for liver in HOAA treated group showed a decrease at day 1. Among blood parameters, white blood cells increased in HOAA treated group at day 1 and in both OAA and HOAA groups at day 28. Mean corpuscular hemoglobin (MCH) and mean cell volume (MCV) also showed increases in the HOAA treated rats at days 7 and 28. Serum lactate dehydrogenase (LDH) decreased in both OAA and HOAA treated rats at day 1, while at day 7 the decrease was confined only to the HOAA group. Serum glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) activities also decreased at most of the time points. Liver mitochondrial ATPase activity decreased in the HOAA group at day 7 and in the OAA group at day 28. Among serum immunoglobulins, IgA levels increased throughout the study but the changes were more pronounced in HOAA treated rats. Splenic T-lymphocyte number decreased in the HOAA treated rats at day 1, recovered at day 7, and then showed an increase at day 28. The B-cell population remained steady at all time points. The T-helper and T-suppressor cell numbers in both OAA and HOAA groups decreased at day 1. However, at days 7 and 28, T-helper cell numbers increased in HOAA group, whereas T-suppressor cells showed an increase in both OAA and HOAA treated rats at day 28. The changes observed as a result of exposure to OAA and HOAA and more so by HOAA, further support that fatty acid anilides may play a role in the pathogenesis of TOS.