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Acute myocardial infarction (AMI) is still one of the most common causes of death worldwide. In recent years, for diagnosis of myocardial ischemia, a new parameter, called ischemia modified albumin (IMA), which is thought to be more advantageous than common methods, has been researched. In this study, systematic analysis of parameters considered to be related to myocardial ischemia has been performed, comparing between control and myocardial ischemia groups. We selected 40 patients with AMI and 25 healthy controls for this study. Ischemia modified albumin levels, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) antioxidant enzyme activities and non-enzymatic antioxidants such as retinol, α-tocopherol, β-carotene and ascorbic acid levels were investigated in both groups. Glutathione (GSH) and malondialdehyde (MDA) levels, which are indicators of oxidative stress, were compared between patient and control groups. Ischemia modified albumin levels were found significantly higher in the AMI diagnosed group when compared with controls. The MDA level was elevated in the patient group, whereas the GSH level was decreased. SOD, GPx and CAT enzyme levels were decreased in the patient group, where it could be presumed that oxidative stress causes the cardiovascular diseases. Due to the increased oxidative stress, non-enzymatic and enzymatic antioxidant capacity was affected. Systematic investigation of parameters related to myocardial infarction has been performed, and it is believed that such parameters can contribute to protection and early diagnosis of AMI and understanding the mechanism of development of the disease.

The elimination of cisplatin ototoxicity is an ongoing concern. This experimental study was undertaken to investigate the effect of oral erdosteine in ameliorating cisplatin-induced ototoxicity. Twenty-eight adult female Wistar albino rats were randomly divided into four equal groups. Group A received an oral carrier vehicle of the drug erdosteine with 0.2 ml of 0.9% saline. Group B was administered only erdosteine (per oral 10 mg/kg twice a day) for 6 days. Group C was injected with cisplatin intraperitoneally (i.p.) on day 0 (16 mg/kg body weight), once only. Group D was given erdosteine (per oral 10 mg/kg/day) 1 day before and for 5 days consecutively after cisplatin injection (16 mg/kg, i.p.). Distortion product otoacoustic emissions (DPOAEs) were elicited in different frequency regions, ranging from 1,001 to 6,299 Hz as DPgram and input/output (I/O) functions from the control and experimental animals. All experimental animals were killed under general anesthesia on day 5, following the last otoacoustic emission measurements. Prior to death, blood samples were drawn for measurement of superoxide dismutase, xanthine oxidase (XO), malondialdehyde and nitric oxide. Initial DPgram and I/O function baseline measurements were similar in all groups prior to any drug administration ( P>0.05). On day 5, intra-subject measurement parameters of DPgrams and I/O functions in the cisplatin group showed significant deterioration ( P <0.05). The other groups revealed no differences between their pre- and post-test drug administration DPgrams and I/O functions at any test frequency ( P>0.05). Comparison of the amplitudes of DPgrams and I/O functions between the cisplatin and control groups showed significant changes ( P <0.05). Biochemical studies noted an increased XO activity following cisplatin administration ( P <0.007). The other biochemical results did not show significant differences between the study and control groups. This study demonstrates that, in rats, erdosteine is protective for cochlear function against the disruptive effects of cisplatin as measured by DPOAEs.

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 PB / 0.05). Erdosteine treatment with rotenone led to an increase in catalase (CAT) and superoxide dismutase (SOD) activities in comparison with the rotenone group PB / 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.

Caffeic acid phenethyl ester (CAPE) is a phenolic active component of propolis of honeybee hives and reduces heart rate and blood pressure in rats. The objective of this study was to investigate the role of vagal activity and atropine blockage on the bradycardic and hypotensive effects of CAPE in rats. The rats were divided into five groups (n = 8). Saline and vehicle (10% ethanol) of CAPE were given to the first and second groups, respectively. Group 3 was treated with 5 mg/kg CAPE. Group 4 bivagotomized and treated with 5 mg/kg CAPE. Group 5 treated with atropine (5 microg/microL/min) continuously and treated with CAPE. The electrophysiological monitoring was done for each experiment under urethane anesthetize. As a result, CAPE caused intense and transient bradycardia and hypotension. Vagotomy completely abolished bradycardia occurred via CAPE injection; however atropine attenuated bradycardic effects of CAPE. On the other hand, hypotensive effect of CAPE was affected from neither bilateral vagotomy nor atropine treatment. It was thought that CAPE may exert its effects on heart rate via a central parasympathetic control mechanism, but not on central parasympathetic blood pressure control system.