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Abstract
BackgroundExposure to pesticides and industrial toxins are implicated in cardiovascular disease. Paraquat (PAR) is a toxic chemical widely used as an herbicide in developing countries and described as a major suicide agent. The hypothesis tested here is that PAR induced myocardial dysfunction may be attributed to altered mechanisms of Ca2+ transport which are in turn possibly linked to oxidative stress. The mechanisms of PAR induced myocardial dysfunction and the impact of antioxidant protection was investigated in rat ventricular myocytes.MethodologyForty adult male Wistar rats were divided into 4 groups receiving the following daily intraperitoneal injections for 3 weeks: Group 1 PAR (10 mg/kg), Control Group 2 saline, Group 3 vitamin E (100 mg/kg) and Group 4 PAR (10 mg/kg) and vitamin E (100 mg/kg). Ventricular action potentials were measured in isolated perfused heart, shortening and intracellular Ca2+ in electrically stimulated ventricular myocytes by video edge detection and fluorescence photometry techniques, and superoxide dismutase (SOD) and catalase (CAT) levels in heart tissue.Principal FindingsSpontaneous heart rate, resting cell length, time to peak (TPK) and time to half (THALF) relaxation of myocyte shortening were unaltered. Amplitude of shortening was significantly reduced in PAR treated rats (4.99±0.26%) and was normalized by vitamin E (7.46±0.44%) compared to controls (7.87±0.52%). PAR significantly increased myocytes resting intracellular Ca2+ whilst TPK and THALF decay and amplitude of the Ca2+ transient were unaltered. The fura-2–cell length trajectory during the relaxation of the twitch contraction was significantly altered in myocytes from PAR treated rats compared to controls suggesting altered myofilament sensitivity to Ca2+ as it was normalized by vitamin E treatment. A significant increase in SOD and CAT activities was observed in both PAR and vitamin E plus PAR groups.ConclusionsPAR exposure compromised rats heart function and ameliorated by vitamin E treatment.
Highlights
Cardiovascular disease is the major cause of premature mortality in both the developed and developing world
It is noteworthy that a number of risk factors which are associated with cardiovascular disease may be linked, at least in part, by oxidative stress
Mitochondrial respiration, enzymatic reactions, and inflammatory response may play a collective role in balancing the production of reactive oxygen species (ROS), and endogenous antioxidant defense system composed of antioxidant molecules and enzymes to counteract the damaging effects of ROS by converting more reactive species to less reactive and less damaging forms [6,7,8]
Summary
Cardiovascular disease is the major cause of premature mortality in both the developed and developing world. Oxidative stress can lead to dysfunction in endothelial cells, monocytes and vascular smooth muscle cells as well as mitochondrial damage [1,2]. A number of mechanisms have been postulated for oxidative stressinduced myopathic changes, including mitochondrial damage, defective mechanimsms of Ca2+ transport, oxidative modification of essential cardiac contractile proteins, and direct cardiac toxicity of ROS [7,8,9], the mechanisms of which underlie ‘‘oxidative cardiomyopathy’’ have not been clearly elucidated. The hypothesis tested here is that PAR induced myocardial dysfunction may be attributed to altered mechanisms of Ca2+ transport which are in turn possibly linked to oxidative stress. The mechanisms of PAR induced myocardial dysfunction and the impact of antioxidant protection was investigated in rat ventricular myocytes
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