Comparison of the effects of two legal blood alcohol limits: the presence of alcohol in traffic accidents according to category of driver in Izmir, Turkey.

OBJECTIVES: Under existing Turkish road traffic law, there are 2 different blood alcohol concentration (BAC) limits allowed for drivers in 2013: zero blood alcohol and ≤0.50 g/L. All public transport, taxi, commercial, and official vehicle drivers must maintain a zero blood alcohol concentration while driving. Private vehicle drivers must maintain a BAC of 0.50 g/L or lower. The aim of the recent study was to evaluate the effect of these 2 legal blood alcohol limits on nonfatal traffic accidents that occurred due to the driver being under the influence of alcohol. METHODS: This retrospective study was performed to evaluate the blood alcohol concentration of 224 drivers in nonfatal road accidents between June 2010 and July 2011 using headspace gas chromatography at the Izmir Forensic Medicine Group Presidency, Turkey. All cases evaluated by the toxicology department were entered into a database. We used descriptive statistics, χ(2) test, and independent sampling test to analyze the data. RESULTS: The total number of drivers involved in nonfatal traffic accidents was 224; 191 were private vehicle drivers and 33 were public transport, taxi, commercial, and official vehicle drivers. In the present study, alcohol was detected in the blood of about 27.2% (n = 61) of the 224 drivers. Sixty (31.4%) private vehicle drivers involved in nonfatal traffic accidents tested positive for alcohol. BAC values were also above the legal limit (0.50 g/L) in 27.7% (n = 53) of private vehicle drivers. However, the BAC was above the legal limit in only 3% (n = 1) of public transport, commercial, and official vehicle drivers involved in nonfatal traffic accidents. These results showed that private vehicle drivers subject to a BAC limit of ≤0.50 g/L were significantly associated with an increased risk of nonfatal accident involvement than drivers subject to a zero BAC limit (odds ratio [OR] = 12.29, 95% confidence interval [CI], 1.64-92.22; Fisher's exact test, P <.001). Mean BAC in private vehicle drivers subject to a 0.50 g/L level (52.60 mg/dl ± 94.84) was significantly higher than that of drivers subject to a zero alcohol level (10.76 mg/dl ± 61.80; t = 2.44, P <.001). CONCLUSION: In light of our results, lowering the BAC limit for private vehicle drivers may reduce the level of driving under the influence of alcohol. A change in the law will decrease the rates of alcohol-related road accidents in Turkey.

The role of reactive oxygen species and oxidative stress in carbon monoxide toxicity: an in-depth analysis.

The underlying mechanism of the central nervous system (CNS) injury after acute carbon monoxide (CO) poisoning is interlaced with multiple factors including apoptosis, abnormal inflammatory responses, hypoxia, and ischemia/reperfusion-like problems. One of the current hypotheses with regard to the molecular mechanism of CO poisoning is the oxidative injury induced by reactive oxygen species, free radicals, and neuronal nitric oxide. Up to now, the relevant mechanism of this injury remains poorly understood. The weakening of antioxidant systems and the increase of lipid peroxidation in the CNS have been implicated, however. Accordingly, in this review, we will highlight the relationship between oxidative stress and CO poisoning from the perspective of forensic toxicology and molecular toxicology.

The forensic deaths caused by pesticide poisoning between the years 2006 and 2009 in Izmir, Turkey.

Pesticide poisoning is still a significant health problem in Turkey. We conducted a retrospective study of autopsy cases at Izmir Branch of the Council of Forensic Medicine to describe the characteristics of deaths caused by pesticide poisoning between 2006 and 2009. The distributions of the cases according to gender and age were as follows: men 74.1% (n = 40, mean [±SD] age, 44.7 ± 14.1), women 25.9% (n = 14, mean [±SD] age, 39.2 ± 18.9). The majority of pesticide-poisoning deaths were suicides (n = 43, 80%) followed by accidents (n = 4, 8%) and homicide (n = 1, 2%). The manner of death could not be determined in six cases (11%). Suicides mostly occurred at home (n = 26, 63%) (p < 0.05). Methomyl was the most frequent pesticide (n = 9, 17%) among the all cases. This study reported that most of the pesticides found in poisoning cases were highly hazardous types. Combined efforts of medical professionals and law makers are needed for enacting strict laws against highly hazardous pesticides.

Protective effect of caffeic acid phenethyl ester (CAPE) administration on cisplatin-induced oxidative damage to liver in rat.

Cisplatin is one of the most active cytotoxic agents in the treatment of cancer. High doses of cisplatin have also been known to produce hepatotoxicity. Several studies suggest that supplementation with an antioxidant can influence cisplatin-induced hepatotoxicity. The present study was designed to determine the effects of cisplatin on the liver oxidant/antioxidant system, and the possible protective effects of caffeic acid phenethyl ester (CAPE) on liver toxicity induced by cisplatin. Twenty-four adult female Wistar albino rats were divided into four groups of six rats each: control, cisplatin, CAPE, and cisplatin+CAPE. Cisplatin and CAPE were injected intraperitoneally. Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), myeloperoxidase (MPO), xanthine oxidase (XO), adenosine deaminase (ADA), and the levels of malondialdehyde and nitric oxide (NO). The activities of SOD and GSH-Px increased in the cisplatin+CAPE and CAPE groups compared with the cisplatin group. CAT activity was higher in the cisplatin +CAPE group than the other three groups. XO activity was lower in the cisplatin group than the control group. MPO activity was also increased in the cisplatin group compared to the control and CAPE groups. It can be concluded that CAPE may prevent cisplatin-induced oxidative changes in liver by strengthening the antioxidant defence system by reducing reactive oxygen species and increasing antioxidant enzyme activities.

Protective effects of erdosteine on rotenone-induced oxidant injury in liver tissue.

Rotenone, an insecticide of botanical origin, causes toxicity through inhibition of complex I of the respiratory chain in mitochondria. This study was undertaken to determine whether rotenone-induced liver oxidant injury is prevented by erdosteine, a mucolytic agent showing antioxidant properties. There were four groups of Male Wistar Albino rats: group one was untreated as control; the other groups were treated with erdosteine (50 mg/kg per day, orally), rotenone (2.5 mg/mL once and 1 mL/kg per day for 60 days, i.p.) or rotenone plus erdosteine, respectively. Rotenone treatment without erdosteine increased xanthine oxidase (XO) enzyme activity and also increased lipid peroxidation in liver tissue (P < 0.05). The rats treated with rotenone plus erdosteine produced a significant decrease in lipid peroxidation and XO activities in comparison with rotenone group (P < 0.05). Erdosteine treatment with rotenone led to an increase in catalase (CAT) and superoxide dismutase (SOD) activities in comparison with the rotenone group (P < 0.05). There was no significant difference in nitric oxide (NO) level between groups. There were negative correlations between CAT activity and malondialdehyde (MDA) level (r = -0.934, P < 0.05) with between CAT and SOD activities (r = -0.714, P < 0.05), and a positive correlation between SOD activity and MDA level (r = 0.828, P < 0.05) in rotenone group. In the rotenone plus erdosteine group, there was a negative correlation between XO activity and NO level in liver tissue (r = -0.833, P < 0.05). In the light of these findings, erdosteine may be a protective agent for rotenone-induced liver oxidative injury in rats.