Research Article Open Access Volume 3 • Issue 4 • 1000176 J Environ Anal Toxicol ISSN: 2161-0525 JEAT, an open access journal Open Access Research Article Environmental & Analytical Toxicology Ismail et al., J Environ Anal Toxicol 2013, 3:4 http://dx.doi.org/10.4172/2161-0525.1000176 *Corresponding author: Samah F. Ibrahim, Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Ain Shams University, Egypt, E-mail: samahibraheem@yahoo.com Received May 19, 2013; Accepted June 24, 2013; Published June 26, 2013 Citation: Ismail MM, El-Ghamry H, Shaker OG, Fawzi MM, Ibrahim SF (2013) Some Biomarkers in Carbon Monoxide-Induced Cardiotoxicity. J Environ Anal Toxicol 3: 176. doi:10.4172/2161-0525.1000176 Copyright: © 2013 Ismail MM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Some Biomarkers in Carbon Monoxide-Induced Cardiotoxicity Manal M. Ismail 1 , Hoda El-Ghamry 1 , Olfat G. Shaker 2 , Marwa M. Fawzi and Samah F. Ibrahim 1 * 1 Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Ain Shams University, Egypt 2 Medical Biochemistry-Faculty of Medicine-Cairo University, Egypt Keywords: Carbon monoxide; Cardiotoxicity; Oxidative stress Introduction Carbon monoxide (CO) is a common cause of morbidity and the most common cause of mortality from poisoning in the United Kingdom [1] and the United States [2]. An Egyptian study performed by the Poison Control Center (PCC), Ain Shams University Hospitals in Cairo, showed that CO poisoning represented the 6 th most frequent toxic exposure (2.28%) out of 25,555 cases admitted to PCC in 2004 [3]. CO induced myocardial damage is not completely understood as a clinical entity in terms of both pathophysiology and clinical features [4]. In carbon monoxide poisoned patients, an altered balance between reactive oxygen species and antioxidant levels has been reported [5]. Free radicals and oxidative stress are among factors involved in pathogenesis of acute carbon monoxide poisoning and particularly appear to have a role in carbon monoxide induced cardio-toxicity [6]. Carbon monoxide cardiotoxicity can be evaluated by various cardiac enzymes such as troponin I and beta natriuretic peptide [7,2]. Aim of the Work e present study aimed at the detection of the cardiac effects of carbon monoxide toxicity through the estimation of cardiac biomarkers in "CO-exposed subjects", to report the oxidative stress effects on the heart of acute carbon monoxide poisoned patients and its relationship to cardiac biomarkers. Methodology is case control study was conducted in Poison Control Center, Ain Shams university Hospital, Cairo, Egypt. Patients with coronary artery disease or other known heart disease, patients with renal failure and individuals subjected to drugs or supplements with antioxidant effect as well as smoker subjects were excluded. is study was conducted on 50 patients diagnosed as acute carbon monoxide poisoning according to medical history, examination, and/or COHb level>3% at the time of presentation. ey were 30 males and 20 females. eir age ranged between 15- 45 years (26.5 ± 8.3 years). Apparently healthy 40 individuals, 20 males and 20 females, matched for age and sex were the control group. Consent for examination was taken from these subjects. On admission to the emergency department, blood samples were withdrawn from patients, aſter detailed clinical examination, to perform the following investigations; blood gases analysis, troponin I, BNP, SOD, MDA and (NO) synthase products (nitrate & nitrite) levels were measured. Baseline 12-lead ECGs were recorded with a paper speed of 25mm/s from each of the patients at the admission. Arterial blood gases and Carboxyhemoglobin measurements were Abstract Background: Myocardial injury is a frequent consequence of carbon monoxide (CO) poisoning. Oxidative stress affection seems to be a relevant mechanism in the patho-physiology of patients with acute CO poisoning. Methodology: Cardiovascular system examination and Electrocardiography (ECG) were performed for fifty CO intoxicated patients admitted to Poison Control Center, Ain Shams university Hospital for whom some oxidative stress indices have been investigated through the assessment of plasma level of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO). Both cardiac enzymes; troponin I and beta natriuretic peptide (BNP) have been also assessed in addition to carboxyhemoglobin (COHb) levels. The investigated parameters were compared with those of 40 non-smoker healthy controls (comparable in terms of age and gender). Results: ECG changes were present in 96% of patients, whereas only 4% had a normal ECG. In intoxicated patients, a statistical significant increase in plasma level of COHb level, MDA, NO, troponin I, and BNP peptide was reported compared to control individuals, while SOD enzyme was significantly decreased. BNP showed a significant positive correlation with COHb level and a negative correlation with SOD, while SOD showed a significant negative correlation with COHb level. Conclusions and recommendations: Myocardial injury occurs frequently in patients hospitalized for CO poisoning. The oxidative stress indices are significantly affected after acute CO poisoning. We suggested that such affection could be partially mediated by CO. Patients admitted to the hospital with CO poisoning should have a baseline ECG and serial cardiac biomarkers.