Biological monitoring of fuel stations workers occupationally exposed to petroleum products

The increased use of petroleum products in automobiles and industry has led to the deterioration in air quality and human health. Petrol [or gasoline] is a volatile and inflammable petroleum derived liquid mixture primarily used for internal combustion of engines. Occupational exposure to gasoline and air pollutant from vehicular sources are relatively unexplored. The main purpose of this study was conducting biological monitoring for petrol workers occupationally exposed to petroleum product and air pollutants. The study was conducted on fifty male workers employed in petrol filler stations and fifty subjects were recruited as a control group matched for age, sex and socio-economic status. Results revealed that presence of high significant association in the levels of liver enzymes and some haematological changes among exposed workers. In addition to the significant decline in the lung function. Also significant increase in urinary phenol as a biomarker of benzene exposure was found. Sulphur dioxide nitrogen dioxide, carbon dioxide and carbon monoxide did not exceed the standards indoor air quality guidelines. However, particulate matter exceeded the limits as indoor air quality guidelines. This study demonstrated that it is possible to detect human health risks at an early stage using sensitive techniques. It is concluded that petrol pump workers should be carefully monitored and should take adequate protective measures to prevent long term effects

Clinical significance of measurements of serum and urinary thrombomodulin and serum e-selectin in diabetic patients with and without complications

Serum and urinary levels of soluble thrombomodulin [TM] and the serum levels of the soluble leucocyte adhesion molecule E-selectin, were measured in 80 diabelic patients. Fourty patients with insulm-dependent diabetes mellitus [IDDM] were divided into 20 non-complicated patients [group I] and 20 complicated patients [group II]. Ten age-matched healthy subjects were used as a control [group III] for the IDDM patients. Another 40 patients with non-insulin-dependent diabetes mellitus [NIDDM] comprised 20 non-complicated patients [group IV] and 20 complicated patients [group V]. Ten more age-matched healthy subjects were selected as a control [group VI] for the NIDDM patients. Serum and urinary concentrations of TM were significantly higher in diabetic patients compared with controls. Moreover, serum and urinary TM levels were significantly increased in complicated IDDM and NIDDM patients compared with the non-complicaied patients and the control subjects. Similarly, serum concentrations of E-selectin were found to be significantly higher in complicated diabetic patients versus the non-complicated patients and the control groups. In all diabetic patients of the four studied groups and in each separale group, serum and urinary levels of TM and serum E-selectin concentrations correlated positively with the duration of diabetes, fasting and postprandial blood glucose, HbA[IC] and urinary albumin excretion. A significant positive correlation was also found between urinary and serum levels of TM in the four studied groups of patients. Furthermore, serum and urinary levels of TM together with serum E-selectin concentrations correlated positively with the frequency of complications in complicated IDDM and NIDDM patients. The results suggest that serum and urinary TM levels could be a sensitive and predictive marker for the generalized vascular endothelial mjury induced by hyperglycemia and/or premicroangiopathy in diabetic patients. The present data point to a functional role for the soluble leucocyte adhesion molecule E-selectin in the development and progressions! complications in diabetic patients. The results also indicate that the concentrations of TM and E-selectin may be retated to metabolic control

Central versus peripheral actions of adrenomedullin in a hypertensive rat model

Adrenomedullin [AM] is a peptide with potent vasorelaxing and natriuretic properties originally isolated from human pheochromocytoma. It may function as a circulating hormone that is involved in the regulation of cardiovascular system, renal function and hormone secretion. It has been observed that the hypotensive effect of AM in the periphery is not matched by a similar effect when injected centrally. The mechanisms involved in the peripheral hypotensive and central hypertensive actions of AM in normal rats are controversial and diverse; moreover in hypertension the underlying mechanisms are not tackled till now. 120 male albino rats were used in this study to assess the mechanisms involved in the peripheral versus the central actions of AM in the rat model. Hypertension was induced in 90 rats using NG-nitro-L-arginine ester [L-NAME] and ten normal rats were used as a control group. The peripheral and central actions of AM were tested in the hypertensive rats and in another 20 normal rats. The 90 hypertensive rats were divided into nine equal groups. Peripherally, AM was either injected alone [group I-A] or following a two-weeks of oral administration of prazosin [0.55 mg/kg/day], propranolol [14.4 mg/kg/day], valsartan [14.4 mg/kg/day] or isosorbide dinitrate [10.4 mg/kg/day] [groups II-A to V-A respectively]. Centrally, AM was either injected intracerebroventricularly [icv] alone [group I-B] or following a bolus icv injection of saralain [10 micro g] [group II-B] or after a two-weeks of oral administration of prazosin [0.55 mg/kg/day] or clonidine [18 micro g/kg/day] [group III-B and IV-B respectively]. Mean arterial blood pressure [MABP], plasma renin activity [PRA] and aldosterone level values were compared before and after AM injection in the same rate of each group. A 40.6% drop in MABP was elicited in normal rats injected peripherally with AM. This drop was attenuated to 18.6% in L-NAME hypertensive rats. The percent age drop in MABP in hypertensive rats pretreated with isosorbide dinitrate [43.3%] was comparable to that observed in normal rats when AM was injected intravenously to both groups [p=0.999]. A significant decrease in PRA and aldosterone level was produced in hypertensive rats pretreated with various drugs following the peripheral administration of AM as compared to their pre-injection values. On the other hand, a significant further increase in MABP was obtained following the icv injection of AM to L-NAME hypertensive rats pretreated with saralazin [P=0.000]. The changes observed in MABP, PRA and aldosterone level after the central administration of AM to hyptertensive rats pretreated with either clonidine or prazosin were insignificant as compared to their pre-injection values. This study suggests that the peripheral vasodilator effect of AM is mediated partially via nitric oxide release or probably by other mechanisms. The central hypertensive response to AM in the L-NAME rat model is probably not mediated by angiotensin-II receptors. It could be through enhancing the central sympathetic discharge via an action on either alpha 1, alpha 2 or the suggested imidazoline receptors located centrally. Finally, AM is supposed to be involved in the physiological resetting of renin-angiotensin-aldosterone system possibly secondary to changes in either catecholamines discharge or nitric oxide level. These results were discussed

influence of experimentally induce, non-insulin dependent diabetes on the extent of myocardial injury in a canine ischaemia-reperfusion model

Diabetes mellitus is a well known risk factor for coronary artery disease and subsequent myocardial infarction. The present study evaluated the effect of short term [12 weeks] experimentally induced non-insulin-requiring diabetes on the extent of myocardial injury in a canine ischaemia-reperfusion model and investigated the underlying biochemical mechanisms. Non-insulin-dependent diabetes was induced in 10 dogs by the streptozotocin-alloxan method and another 10 dogs were used as controls. On the day of the experiment, dogs of either group were weighted and blood samples were withdrawn from the anticubital vein for biochemical and lipid determinations. Dogs were then anaesthetised and myocardial infarction was provoked by occluding the left anterior descending coronary artery [LAD] for 1 hour followed by 3 hours reperfusion. Biopsies were taken from the center of the LAD bed before and then after the 4 hours of the whole occlusion/reperfusion technique. Twelve weeks following diabetes induction, diabetic dogs had higher fasting blood glucose, fructosamine, cholesterol, triglycerides, and apo B concentrations than control dogs. Plasma insulin level was significantly lower in diabetic dogs than controls. Also, plasma antioxidants vitamin E and A were significantly lower in diabetics than in controls on the day of the surgical procedure. Capillaries of the diabetic myocardium showed thickening of basal lamina. The diabetic cardiocytes revealed scalloping of sarcolemma and changes in the Z line in the form of thickening, irregularity and loss of alignment. Light bands were seen in many areas along the myofibrils. After ischaemia-reperfusion, severe ultrastructural changes were observed in the diabetic cardiocytes. Myofilaments showed disruption, lysis and fragmentation. Mitochondrial changes and widening of intercalated discs were also noticed. From the previous study, we cannot identify exactly the mechanism[s] by which diabetes aggravated myocardial injury. The results nevertheless suggest that one reason why myocardial ischaemia is less well tolerated in diabetics than in non-diabetics is likely to be by inducing myocardial ultrastructural changes. This may partly explain the poor prognosis of myocardial infarction in diabetic persons