Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats

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.

Dietary antioxidants at supranutritional doses improve oxidative status and reduce the negative effects of heat stress in sheep1,2

“…This increase in heart rate may be associated with increased metabolic activity, as the sheep were fed after the 0900 h (basal measurements) measurements of physiological parameters. Interestingly, the heart rate was reduced by the antioxidant supplementation irrespective of thermal treatment, which may be explained by the beneficial effects of Vit E on the cardiac autonomic nervous system as has been reported in rats and humans (Behrens et al, 1986;Manzella et al, 2001;Fahim et al, 2013) In general, exposure of sheep to high ambient temperatures results in decline in feed intake along with the increased respiration rate and rectal temperature, compromising the efforts to dissipate heat (Marai et al, 2007). In this study, we found 13% decline in feed intake of CTRL group when exposed to HS.…”

High dietary selenium and vitamin E supplementation ameliorates the impacts of heat load on oxidative status and acid-base balance in sheep1,2

“…This may also explain beneficial effects of antioxidant (Vit E) feeding during HS other than reducing the OS in sheep. The beneficial effects of Vit E on the cardiac autonomic nervous system have also been reported to reduce heart rate in rats and humans (Behrens et al, 1986;Manzella et al, 2001;Fahim et al, 2013). An increase in the parasympathetic tone of the autonomic nervous system would be consistent with an improvement in GIT function.…”

Cardiac-Specific Knockout of ETA Receptor Mitigates Paraquat-Induced Cardiac Contractile Dysfunction

“…Recent evidence also revealed compromised cardiac structure and function Jiaxing Wang, Songhe Lu and Qijun Zheng have contributed equally to this work. including cardiac enlargement, contractile dysfunction and bradycardia [10][11][12][13][14]. Up-to-date, several mechanisms have been postulated for paraquat-induced cellular injury including oxidative stress, disturbed mitochondrial oxidative phosphorylation and respiration events [15][16][17][18][19].…”