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Carbon monoxide (CO) poisoning is a significant cause of death especially in developing countries. The current study investigated cardioprotective effects of insulin in CO-poisoned rats. Male rats were exposed to 3000 ppm CO for 1 h. Insulin (100 and 120 U/kg intraperitoneally) was immediately administered after CO exposure and on the next 4 days, on a daily basis (a total of 5 doses). On day 5, animals were euthanized, and the hearts were harvested for Western blotting and histopathological studies. The electrocardiograms (ECG) were recorded postexposure to CO and after the completion of insulin treatment period. Histopathological evaluations showed reduction of myocardial necrosis in insulin-treated animals compared to controls. BAX/BCL2 ratio, as a proapoptotic index, was significantly reduced in treatment groups (p < 0.01). The ECG findings showed no differences among groups; also, compared to control animals, myocardial Akt levels were not markedly affected by insulin. The current study showed that insulin significantly reduces myocardial necrotic and apoptotic indices in CO-poisoned rats. [ABSTRACT FROM AUTHOR]

In real life, consumers are exposed to complex mixtures of chemicals via food, water and commercial products consumption. Since risk assessment usually focuses on individual compounds, the current regulatory approach doesn't assess the overall risk of chemicals present in a mixture. This study will evaluate the cumulative toxicity of mixtures of different classes of pesticides and mixtures of different classes of pesticides together with food additives (FAs) and common consumer product chemicals using realistic doses after long-term exposure. Groups of Sprague Dawley (CD-SD) rats (20 males and 20 females) will be treated with mixtures of pesticides or mixtures of pesticides together with FAs and common consumer product chemicals in 0.0, 0.25 × acceptable daily intake (ADI)/tolerable daily intake (TDI), ADI/TDI and 5 × ADI/TDI doses for 104 weeks. All animals will be examined every day for signs of morbidity and mortality. Clinical chemistry hematological parameters, serum hormone levels, biomarkers of oxidative stress, cardiotoxicity, genotoxicity, urinalysis and echocardiographic tests will be assessed periodically at 6 month intervals. At 3-month intervals, ophthalmological examination, test for sensory reactivity to different types of stimuli, together with assessment of learning abilities and memory performance of the adult and ageing animals will be conducted. After 24 months, animals will be necropsied, and internal organs will be histopathologically examined. If the hypothesis of an increased risk or a new hazard not currently identified from cumulative exposure to multiple chemicals was observed, this will provide further information to public authorities and research communities supporting the need of replacing current singlecompound risk assessment by a more robust cumulative risk assessment paradigm. [ABSTRACT FROM AUTHOR]

Lethal cardiac complications leading to death and various arrhythmias have been reported after organophosphate and/or carbamate poisonings. The present study focuses on the long-term effects of repeated low-level exposure to diazinon, propoxur, and chlorpyrifos (CPF) on cardiac function in rabbits. The yearly based experimental scheme of exposure consisted of two oral administration periods, lasting 3 months and 1 month each, interrupted by an 8-month washout period (total duration 12 months). At the end of the experimental scheme, the rabbits underwent an echocardiographic evaluation under sedation, after which they were killed and the tissue and serum samples were collected. A mild localized cardiotoxic effect was established by echocardiography for the three pesticides tested. Severe histological alterations were identified, especially in the diazinon-treated animals in agreement with increased persistence of this pesticide established in the cardiac tissue. In addition, all pesticides tested increased the oxidative stress and oxidative modifications in the genomic DNA content of the cardiac tissues, each one following a distinct mechanism. [ABSTRACT FROM PUBLISHER]

Brugada syndrome is an inherited autosomal dominant-type disease characterized by ST-segment abnormalities and increased fatal ventricular tachyarrhythmias. We hereby present a 57-years-old patient with no symptoms or history of cardiovascular disease, diagnosed with febrile respiratory infection (39°C). Electrocardiographic (ECG) findings were typical of Brugada-like type I syndrome that gradually turned to Brugada type II and III, following fever remission, and finally became normal. Other clinical evaluation tests (echocardiographic evaluation, treadmill stress test, Holter ECG, procainamide provocation test) did not relate to Brugada syndrome. [ABSTRACT FROM AUTHOR]

Abstract: Oxidative stress has been shown to increase after acute myocardial infarction and during coronary reperfusion. Allopurinol inhibits xanthine oxidase, an enzyme involved in reperfusion injury. In this study, 40 patients with ST elevation myocardial infarction and symptoms'' onset 3–12h, who underwent primary coronary intervention, were administered either allopurinol (loading dose 400mg followed by 100mg for 1month — group A, 21 patients), or placebo (group B). Allopurinol resulted in a more effective ST-E recovery (P <0.05 for all comparisons) and lower peak values of troponin I (P =0.04), CPK (P =0.01) and CK-MB (P =0.03). After 1-month follow-up period, 13% lower incidence of major adverse cardiac events (P =0.002) was also observed in group A, whereas no significant differences in the EF were detected between the groups studied. In our study population, allopurinol administration was beneficial concerning tissue reperfusion, myocardial injury and clinical outcomes. [Copyright &y& Elsevier]