The effects of ubiquinone (CoQ10) on heart tissue in cardiac toxicity related to organophosphate poisoning

Abstract

The aim of this study was to examine the effects of ubiquinone (CoQ10) on heart tissue and erythrocytes in acute organophosphate poisoning (AOP). A total of 20 rabbits were divided into three groups: sham (n = 8), pralidoxime (PAM) + atropine (n = 6), and CoQ10 + PAM + atropine (n = 6). Blood samples were taken from each test subject to measure the values of acetylcholinesterase (AChE), nitric oxide (NO), and malondialdehyde (MDA) in the plasma and erythrocyte before administration of 50 mg/kg dichlorvos by orogastric tube. Blood samples were then taken at 1, 12, and 24 h post-dichlorvos to determine plasma and erythrocyte levels of AChE, NO, and MDA. Sham group received no treatment. PAM + atropine group received 0.05 mg/kg atropine with repeated doses and PAM: first a 30-mg/kg intravenous (IV) bolus, then a 15-mg/kg IV bolus every 4 h. CoQ10 + PAM + atropine group received same dose PAM and atropine and a 50-mg bolus of IV CoQ10. Thoracotomy was performed in all the animals 24 h after poisoning and then heart tissue samples were obtained. At 12 and 24 h, erythrocyte AChE levels in the CoQ10 animals were considerably higher than those in PAM + atropine animals (p = 0.023 and 0.017, respectively). At 12 and 24 h, erythrocyte MDA and NO levels in CoQ10 animals were significantly lower than those in PAM + atropine animals (p < 0.05). Heart tissue AChE levels in CoQ10 animals were considerably higher than those of the sham and PAM + atropine animals (p = 0.001). Heart tissue MDA and NO levels of CoQ10 animals were significantly lower than those of the sham and PAM + atropine animals (p < 0.01). Treatment of AOP with CoQ10 + PAM + atropine in this animal model had a beneficial effect on both erythrocyte and heart tissue lipid peroxidation and AChE activity.

Terbufos-sulfone exacerbates cardiac lesions in diabetic rats: a sub-acute toxicity study

“…The cardiovascular manifestation of OPC poisoning is mainly attributed to acute poisoning (23)(24)(25)(26)(27), which comprises bradycardia or tachycardia or impaired heart rate. There are reports showing an increased level of creatine kinases and lactate dehydrogenases, besides myocardial necrosis (28). The results of the present study reveal that TS causes a leakage of myocyte injury marker enzymes into the serum, as evidenced by the elevated levels of serum CK and LDH.…”

The Effect of Organophosphate Exposure on Neuronal Cell Coenzyme Q10 Status

“…There is a paucity of information available on the ability of CoQ 10 to ameliorate some of the adverse clinical effects associated with OP toxicity. However, a study by Bayir et al [51] reported the ability of CoQ 10 to attenuate OP induced cardiac toxicity. Furthermore, a recent study by Belousova et al [42] demonstrated that CoQ 10 improves neurological function in transient focal brain ischemia in rats [42].…”

Cardiovascular Toxicity of Chlorpyrifos in Female Adult Rats: A Probable Protective Effect of Phytochemical Isoflavones

“…Cardiovascular system affected by OP poisoning, cardiovascular manifestations include hypertension, sinus tachycardia, and bradycardia and reduced heart rate 4 . CF poisoning causes the heart tissue to produce high quantity of free radicals, become sensitive to oxidative stress, and damage 5 , these effects causes cardiovascular changes include an increase in cardiac marker enzymes level in serum; such as lactate dehydrogenase (LDH) and creatinine kinase-MB 6 . Because of CF widespread use, its residues detected in crops and in air 7&8 , which are considered dangerous to the living organisms 9 .…”