Nitric oxide levels during erythroid differentiation in K562 cell line.

Nitric oxide (NO) is endogenous mediator of numerous physiological processes that range from regulation cardiovascular function and neurotransmission to antipathogenic and tumoricidal responses. This study was designed to investigate the possible role of NO during erythroid differentiation in K562 erythroleukemia cells. The chronic myelogenous leukemia (K562) cell line can be triggered in culture to differentiate along the erythrocytic pathway, in response to a variety of stimulatory agents. In this study, K562 cells were induced to synthesize hemoglobin by hemin. We investigated NOx (nitrate+nitrite) levels in uninduced (control) and hemin-induced K562 cell lysates during erythroid differentiation. Our results showed that NO levels decreased significantly on fourth and sixth day both in hemin-induced and control cells; the decrease was, however, more in hemin-induced group than in control group.

Effects of aminoguanidine on glomerular basement membrane thickness and anionic charge in a diabetic rat model.

We investigated the effect of aminoguanidine (AG) administration on GBM thickness, glomerular heparan sulfate (HS) content, and urinary albumin and HS excretion in diabetic rats. After induction of diabetes, female Wistar rats were divided into 2 groups: Group AGDM (n = 11) received 1 g/L aminoguanidine bicarbonate in drinking water, group DC (n = 12) was given only tap water. Control rats received AG (group AGH, n = 8) or tap water (group HC, n = 8). At the end of a period of 8 weeks, urinary albumin and glycosaminoglycan (GAG) excretion was detected. GBM heparan sulfate distribution and count was determined under the electron microscope. The AGDM group had lower urinary albumin and GAG excretion than diabetic controls. GBM thickness was increased in diabetic rats compared to groups of AGDM and HC. In AGDM group alcian blue stained particle distribution and count in the GBM was similar to healthy controls. In conclusion AG prevents the decrease of anionic charged molecules in the GBM and GBM thickening. This can be one of the mechanisms by which AG decreases albuminuria in diabetic rats.

[Evaluation of inferior wall myocardial infarctions by ECG using 5 unipolar retrocardial leads in addition to the standard 12 leads]. / Inferior miyokard infarktüslerinin standart 12 derivasyonlu EKG'ye ilaveten Sirttan (retrokordiyal) kayit edilen ünipolar 5 derivasyon yardimiyla incelenmesi.

OBJECTIVE: This study was planned to evaluate the change patterns in 5 unipolar retrocardial leads (taken from back) in addition to standard 12 leads ECG in subjects with inferior myocardial infarction (IMI) and to see whether these patterns, if there are any, could be useful to assess the cases with IMI. METHODS: A hundred forty two cases were included to study. At first, in order to determine the normal ECG configurations in 5 unipolar retrocardial leads 30 subjects with normal standard 12 lead ECG and normal physical findings were studied. The normal configurations of retrocardial leads were then determined and retrocardial leads were expressed as RE1-5. Later, 60 subjects with chronic IMI and 52 with acute IMI were evaluated. RESULTS: The QS or Qr in VRE1, QR or qR in VRE2, qRs in VRE5 and transitional patterns in VRE3-4 were accepted as normal configurations of the retrocardial leads. Pre- and retrocardial derivations of 60 cases who had old IMI were normal in 21(35%) cases. There were pathologic Q waves in VRE1-VRE2 leads in 5 (8.3%) cases, in VRE3-VRE4 leads in 11(18.3%) cases, in V5-V6 and VRE5 leads in 3 (5%) cases, in V5-V6 and VRE1-VRE5 leads in 12 (20%) cases, in VRE1-VRE4 leads in 8 (13.3%) cases. Pre- and retrocardial leads of 52 cases with acute IMI were normal in 10 (19.5%) cases. There were ST segment depression in V1-V2 and ST segment elevation in VRE-VRE2 leads in 4 (7.6%) cases, ST segment depressions in V3-V4 derivations and ST segment elevations in VRE3-VRE4 leads in 5 (9.6%) cases, ST segment depression in V2-V6, VRE5 leads and ST segment elevation in VRE1-VRE4 leads in 8 (15.3%) cases, ST segment depression in V1-V4 leads and ST segment elevations in RE1-VRE4 in 12 (23%) cases. ST segment depression in V1-V4 leads and ST segment elevation in V5-V6 and VRE1-VRE5 were found in 13 (25%) cases. CONCLUSION: According to ECG findings which were taken from pre- and retrocardial leads of IMI cases were classified as follows; ST elevation or Q wave or both in DII, DIII, AVF(-)+; 1--Pre and retrocardial leads are normal; 2--ST depression in V1 (sometimes ST elevation if there is right ventricular involvement)--V2, ST elevation or Q wave or both in VRE1-VRE2); 3--ST depression in V3-V4 and ST elevation or Q wave or both in VRE3-VRE4); 4--ST depression in V1-V4 and ST elevation or Q wave or both in VRE1-VRE4); 5--ST depression in V1-V4, ST elevation or Q wave or both inV5-V6 and ST elevation or Q wave or both in VRE1-VRE5); 6--ST depression in V1-V6 and ST elevation or Q wave or both in VRE1-VRE4 and ST depression in VRE5). It is concluded that, in addition to standard 12 lead ECG, retrocardial 5 leads could be recorded and interpreted easily. ECG patterns taken from 5 unipolar retrocardial leads in patients with IMI are not homogeneous. Different groups of ECG findings in certain leads were determined. Further investigations to clarify these different groups ECG findings are needed and these might bring a new approach to assess the subjects with IMI.

The effect of losartan and captopril on glomerular basement membrane anionic charge in a diabetic rat model.

OBJECTIVE: Although angiotensin-converting enzyme inhibitors are known to reduce albuminuria by preserving glomerular basement membrane anionic content, the effects of angiotensin II receptor blockage are currently not known. The aim of this study was to evaluate the effects of captopril and losartan on glomerular basement membrane anionic charges in a diabetic rat model. DESIGN: After diabetes induction with streptozotocin, female Wistar rats were divided into three groups: group A, losartan 10 mg/kg by gavage (n = 8); group B, captopril 50 mg/l in drinking water (n = 6); group C, diabetic control rats (n = 8) given only tap water. Group D (eight rats) served as non-diabetic controls. At the end of 8 weeks, erythrocyte membrane charge, serum sialic acid, urinary glycosaminoglycan and albumin were measured and kidney specimens stained with Alcian blue in order to assess basement membrane glycosaminoglycans. RESULTS: Red blood cell anionic charges (ng Alcian blue/ 10(6) red blood cells) were 371.5+/-9.9 for group A, 443.5+/-7.1 for group B, 400.1+/-14.7 for group C, 468.7+/-4 for group D (AD, P<0.01; A>B P<0.01). Albuminuria (microg/day) was 778+/-221 for group A, 719+/-314 for group B, 1724+/-945 for group C, 393+/-263 for group D (A, B

Low dose MK-801 protects against iron-induced oxidative changes in a rat model of focal epilepsy.

We have used chemiluminescence measurements to examine the relationship between free radical formation and excitotoxicity in a post-traumatic epilepsy model. For this purpose, seven days after injecting iron in rat brain cortices, we measured luminol- and lucigenin-enhanced chemiluminescence in different brain regions (ipsilateral cortex, contralateral cortex, hypothalamus and hippocampus). In all brain regions (except contralateral cortices) both luminol- and lucigenin-enhanced chemiluminescence were increased in iron-injected group compared to saline-injected control group. These increases returned to control values in iron-injected rats pretreated with MK-801. Our results suggest that both free radicals and excitatory amino acids play important roles in the development of post-traumatic epilepsy and that MK-801 has protective effects against iron-induced chemiluminescence formation.

NMDA excitotoxicity and free radical generation in rat brain homogenates: application of a chemiluminescence assay.

NMDA, the specific agonist of glutamate gated ion channels permeable to calcium, is implicated as a causal factor in the pathogenesis of several neurobiological disorders such as stroke, seizures, ischemia, and chronic neurodegenerative diseases. On the other hand, evidence on the roles of oxidative mechanisms involved in NMDA-induced neurotoxicity is accumulating. In this study, we have used chemiluminescence measurements as an easy, rapid and sensitive assay to investigate the effects of NMDA and oxidative stress on brain cell vulnerability. Rat brain homogenates were incubated with increasing concentrations of glutamate and NMDA. Production of reactive oxygen species was followed by single photon emission measurements using the specific enhancers luminol and lucigenin. Increases in emission were observed at excitotoxic concentrations of glutamate and NMDA. Other parameters of oxidative stress such as diene conjugates, TBARS and carbonyl groups were also investigated. Our results indicated that chemiluminescence measurements may be used to study involvement of oxidative stress in neurotoxicity.