Oxidative stress, histopathological and haemato-biochemical features in dromedary camels intoxicated with gliotoxin

The aim of the current study was to determine the effect of intravenous administration of gliotoxin on oxidative stress, histopathological and haemato-biochemical features in dromedary camels before injection (0h) and at 1, 24, 48 and 72 hours post injection. Five healthy adult female camels (8-10 years old having 300-350 kg b.wt.) were injected intravenously with gliotoxin (0.025pg/kg b.wt.). Blood samples were collected in plain and heparinised vacutainers at all time points (0, 1, 24, 48 and 72h). The whole blood in heparinised vacutainers was used for estimation of haematological parameters. Obtained sera stored frozen at -30°C until used for estimation of biochemical and oxidative stress biomarkers. Liver and heart tissues were collected from one camel died 24 hours post gliotoxin injection and subjected for histopathological examination. The findings revealed significant increase in the values of ALT, AST, urea, creatinine and neutrophils along with significant reduction in values of total leucocyte count (TLC), total erythrocyte count (TEC), hemoglobin (Hb), lymphocytes percentages, glucose, total proteins, albumin and globulin concentrations in gliotoxin treated camels 1, 24, 48 and 72 hour post gliotoxin injection. Gliotoxin induced significant increase in malondialdehyde (MDA) concentration accompanied with significant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione S-transferase (GST) and glutathione reductase (GR) at all time points post injection. Postmortem examination of the dead camel showed congestion and oedema in both lungs. Histopathological findings revealed presence of homogenous eosinophilic fluid within alveoli and congestion of interalveolar capillaries and within the myocardium. In conclusion, the injected dose of gliotoxin was acutely toxic to camels as reflected on disturbed liver and kidney functions, acceleration of oxidative stress and inhibition of antioxidants enzyme activities.