Cardio- toxicity induced by inhalation of petroleum products-the role of oxidative stress

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCC049

Poster Communications: Cardio- toxicity induced by inhalation of petroleum products-the role of oxidative stress

O. M. Azeez2,1, C. N. Anigbogu1,2, W. A. Saka1,3, R. E. Akhigbe1,4

1. Veterinary Physiology and Pharmacology, University of Ilorin, Ilorin, Kwara, Nigeria. 2. Physiology, College of Medicine University of Lagos, Lagos, Lagos, Nigeria. 3. Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo, Nigeria. 4. Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo, Nigeria.

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OBJECTIVE: To investigate the effect of inhaling diesel, kerosene and petrol on cardiovascular functions and involvement of oxidative stress in Sprague Dawley rats METHODOLOGY: Adult male Sprague-Dawley rats were divided into 4 groups with ten in each group. The animals were acclimatized for two weeks, before the commencement of the study. The control was not exposed to any petroleum product. The diesel, kerosene and petrol sub-groups, were exposed to their corresponding contaminants via inhalation. The diesel, kerosene and petrol groups inhaled diesel, kerosene and petrol, respectively for five minutes once a day in fume chamber for eight weeks. The animals were placed in fume chamber with 1000ml beaker containing 500ml of petroleum products. The difference between the volume before and after the exposure gave the volume consumed. At the end of exposure period, rats were anaesthesized with 1% chloralose and 25% urethane mixture. Blood pressure (BP), heart rate (HR) and Baroreflex response over 30 seconds were measured using blood pressure transducer attached to the polygraph(model 7D); the rate pressure product (RPP) was thereafter calculated. The activities of superoxide dismutase (SOD), catalase (CAT) and concentrations of reduced glutathione (GSH) and Malondialdehyde (MDA) were evaluated in homogenate of lung and heart. The guidelines of the Institution animal ethics Committee was strictly adhered to. RESULTS: There was significant increase in BP, HR and RPP of all treated groups relative to control. There was also significant increase in baroreflex response in diesel and kerosene, but not in petrol-treated when compared with control. The increase in BP and HR persisted in all the treated groups, one week after withdrawal of exposure. There was significant (p<0.05) decrease in the activities of SOD, CAT and GSH and significant (p<0.05) increase in MDA concentration in the serum and tissue homogenate of all treated groups relative to control. The cardiac muscle showed varying degrees of degeneration in the myocytes and the fibres. The lung showed degeneration of parenchyma and the alveolar wall. CONCLUSION: The study showed that oxidative stress induction may have been partly responsible for the cardiotoxicity and alterations of the cardiovascular functions induced by inhalation of petroleum products



Where applicable, experiments conform with Society ethical requirements.

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