The most important characteristic of calcium channels is selective regulation of slow incoming stream of calcium into the cell tissue providing the slow increasement of action potential. Such tissues include smooth muscles of blood vessels, cardiocytes and heart noduses (AV and SA node). Different calcuim antagonists have different effects on previous tissues due to their different chemical formula. Verapamile, Nifedipin and Diltiazem are the most frequently used of all. Their commonest characteristic is blocking the calcium channels causing vasodilatation of blood vessels as well as negative inotropic and chronotropic influence. By blocking the incoming calcium through slow channels of myofibrils of smooth muscles, the antagonists of calcium decrease the quantity of available calcium for contraction which causes vasodilatation. The most famous and most frequently used calcium antagonist is Verapamile. In terms of electrophysiology, Verapamile inhibits action potentials of heart noduses, especially the AV node, where the slow incoming of calcium is the most important for depolarization. Prolongation of the efective refractory period of SA node causes the heart frequency decreasement while prolongation of the effective refractory period of AV node slows down the work of chambers in case of flater and fibrillation of atriums. The molecules of calcium-bonding protein called kalmodulin are located in synaptic endings. Each kalmodulin can bond four calcium ions providing transfer into active calcium-kalmodulin complex which activates the kinase protein. Activated kinase protein starts the exocytosis of neurotransmitters into synaptic gap. Apart from activating kinase protein, calciumkalmodulin complex also starts the activity of calcium pump presynaptic membrane which pumps calcium out of presynaptic ending stopping the further exocytosis of neurotransmitters into synaptic gap. Taking into consideration the fact that opening the calcium channels on membrane of presynaptic ending is necessary to free the neurotransmitter out of the vesicle, the aim of our work is to study whether Verapamile has effects on the membrane of presynaptic endings of sympathetic nervous system checking the level of catecholamine in serum. The experiment was conducted in 6 healthy dogs which were, after 10-minute- infusion (0.9% NaCl), treated with intravenous bolus veramapile injections in three occasions, in every 5 minutes, until the first signs of intoxication had appeared. This caused bradycardia, heart rhythm disorder and blood pressure drop. In order to determine the level of catecholamine, blood was taken sequentially, in every 5 minutes, before the new dose of verapamile was given. Verapamile (given intravenous) significantly decreases the concentration of adrenaline and noradrenaline in the serum of dogs.

Ishrana je jedan od bitnih faktora koji može da dovede do ranijeg gubitka koštane gustine. Unos dovoljne količine voća i povrća, koje sadrže različite karotenoide (karoten, uključujući beta (ß)-kriptoksantin, lutein, likopen, ß-arotin, astakantin i rutin), ima podsticajnu ulogu u osteogenezi. Eksperimenti in vitro ukazuju da jedan od karotenoida, ß-kriptoksantin, ima dvostuku ulogu u homeostazi koštanog tkiva : inhibiše osteoklaste i na taj način smanjuje reapsorpciju koštanog tkiva, a sa druge strane stimulativno deluje na osteoblaste i uvećava koštanu gustinu. Cilj našega rada je bio da utvrdimo da li postoji korelacija između nivoa koštane gustine i nivoa karotenoida. Uradili smo ostodenzitometriju kod 52 žene, izmerili smo ukupni skor karotenoida u ljudskoj koži in vivo pomoću Ramanove spektroskopije. Nakon obrade dobijenih podataka našli smo značajnu negativnu korelaciju između stepena gubitka koštane gustine i nivoa karotenoida (p<0,05). nivoa karotenoida u koži (Skin carotenoid scor) je posledica oksidativnog stresa koja ima reperkusije i na koštano tkivo jer dolazi do povećanja reapsorpcije koštanog tkiva i do povećanja stepena gubitka koštane gustine.

Oksidativni stres predstavlja disbalans u homeostazi egzogenih i endogenih oksidanasa. Prisustvo povećanih koncentracija oksidanasa u ćelijama i ekstracelularnim tečnostima dovodi do spntanih post-translacionih modifikacija proteina i utiče na njihove hemijske, biološke, fizičke i imunogene osobine, i predstavlja deo molekulskih mehanizama mnogih bolesti. Do sada su opisane brojne post-translacione modifikacije proteina u uslovima oksidativnog stresa. Pored direktnog oksidantnog dejstva kiseonikovih i azotnih slobodnih radikala, i brojni drugi oksidansi učestvuju u post-translacionim modifikacijama proteina. Tako se glikaciom i glikoksidacijom stvaraju AGE (advanced glycation end-products), reakcijom sa lipidnim aldehidima i ketonima ALE (advanced lipoxidation end-products), oksidacijom i polimerizacijom AOPP (advanced oxidation protein products), a reakcijom sa ureom i/ ili izocijanskom kiselinom nastaju produkti karabmoilacije proteina. U ovom preglednom članku dat je opis hemijskih modifikacija proteina sa posebnim osvrtom na značaj u patogenetskom mehanizmu razvoja pojedinih bolesti kod čoveka.

Strenuous exercises greatly increase oxygen consumption in the whole body, especially in skeletal muscles. Large part of oxygen consumption is reduced to H2O and ATP, but smaller part (2-5%) results in an increased leakage of electrons from the mitochondrial respiratory chain, forming various reactive oxygen species-ROS (02, H2O,iOH). These free ra- dicals are capable of triggering a chain of damaging biochemical and physiological reactions (oxidative stress, lipid peroxi- dation), as a base for skeletal muscles damage after exercise. MDA (malondialdehyde) is a marker of exercise induced lipid peroxidation process. L-ascorbic acid is a major aqueous-phase antioxidant. To estimate antioxidant role of ascorbic acid we use rate between dehydroascorbate and ascorbate. In this paper those markers of lipid peroxidation (MDA, MDA ind, % ind MDA), and ascorbic acid status (ascorbic acid Asc, ascorbat A, dehidroascorbat DHA, DHA/A) were determinated in 30 stu- dents, in rest and after treadmill running protocol (Bruce Treadmill Protocol). It was found that after the treadmill test, plas- ma MDA level had increased from 3,04 to 4,39 M/L (p<0,0001) and % ind MDA decreased significantly from 35% to 24,7% (p=0,0003). Plasma ascorbic acid was also found to be higher after the treadmill test comparing to rest level (from 55,4 to 67,6 μM/L). DHA/A level in rest was 1,62 and after treadmill test it increased to 2,05 (p=0,0014). These results suggests that strenuous exercise increased process of lipid peroxidation (MDA †, % ind MDA), but in the same time incre- ased ascorbic acid level in plasma and DHA/A rate indicates stronger activation of nonenzymatic antioxidant defense system.

In the last ten years significant progress has been made in understanding of role of neutrophil granulocytes and their enzyme myeloperoxidase in the evolution and complications of atherosclerosis. Myeloperoxidase plays the role in the development of vulnerable plaque associated with the development of acute coronary syndrome. There is much evidence that suggests the role of myeloperoxidase in the development of vulnerable plaque. We investigate the value of myeloperoxidase as marker of the presence of vulnerable plaques in patients with acute coronary syndrome. Myeloperoxidase activity was significantly high in serum of the patients with the diagnosis of acute coronary syndrome as reflection of the presence of vulnerable plaques. Increase in myeloperoxidase activity in serum of patients with the diagnosis of acute coronary syndrome precedes to myocardial damage.

It is well known that intensive physical activity increase the production of reactive species of O and N (RONS), but 2 it is also known that moderate and regular physical activity has influence on antioxidative system adaptation and help in repairing process of oxidative damage. In this paper we estimated markers of lipid peroxidation (MDA, % ind MDA), and antioxidant status (Asc, DHA/A, GSH, CAT, Pex) for 30 students (control group), and 30 professional football players (regular intensive physical activity). In the group of professional sportsman there were significant increase of lipid peroxidation markers (MDA ↑, % ind MDA ↑), which was also followed by an increased antioxidant activity (Asc ↑, DHA/A ↑, GSH ↑, Pex ↑, CAT ≈). We can conclude that chronic physical activity significantly improves antioxidant status using the adaptation process.

Oxidative stress and associated oxidative damage are mediators of vascular injury and inflammation in many cardiovascular diseases, including hypertension, atherosclerosis, ischemic heart disease, diabetes. Xanthine oxidoreductase is one of the enzymes producing free radicals in the cardiovascular system, and it can contribute to the increment of the oxidative stress and, consequently, blood pressure. The xanthine oxidase is a molybdoenzyme capable of catalyzing the oxidation of hypoxanthine and xanthine in the process of purine metabolism. Xanthine oxidase can exist in two interconvertible forms, either as xanthine dehydrogenase or xanthine oxidase. The aim of the paper was investigate the activity xanthine oxidoreductase in the plasma patients with age related cataract, with hypertensive, and with heart failure. Clinical and biochemical researches were carried out in 73 patients with age related cataract, mean age 72±7 years, divided into group with hypertensive (N=35), with heart failure (N=22) and group normotensive and without heart failure (N=16). Plasma xanthine oxidoreductase activity was determined spectrophotometrically by measuring the formation of uric acid from hypoxanthine at 293 nm. The concentration of triglycerides (TG), total cholesterol (TC), LDL-C, HDL-C in plasma were determined. Our findings show a significantly increased activity xanthine oxidoreductase in plasma hypertensive patients (XO 9.18±1.5 U/L) (p< 0.001) and patients with heart failure (XO 10.44±1.53U/L) (p< 0.001), compared with values plasma xanthine oxidoreductase activity in normotensive and patients without heart failure (XOD 6.02±1.4 U/L). Concentrations of plasma TG, TC and LDL-C were elevated in groups with hypertensive and with heart failure, and we to find significant differences with group normotensive and without heart failure values. Elevated activity of plasma xanthine oxidoreductase contribute to the increasåd oxidative stress and may play a role in accelerated atherosclerosis. 

Any kind of ocular lens opacification is well known as cataract. Most cataracts are age-related, so called senile cataract. Cataractogenesis as process involves either pathological and natural aging processes. Chronical oxidative stress is considered as primary factor in age-related cataractogenesis. In this study we measured concentration of lipid hydroperoxides, sulfhydril groups (SH) and entire antioxidative capacity,as well as ocular superoxide dismutase and catalase activity in 11 subjects with diabetes mellitus (DM) type 2 and cataract and in 39 nondiabetic subjects with senile cataract. All patients underwent complete ophthalmological examination before they were surgically treated by phacoemulsifications. 0 During the intervention, aqueous sample in volume 0,2 was aspirated and refrigerated in -20 C and preparated for further biochemical analysis. Parameters of antioxidative power in diabetic subjects with cataract have decreased values (sulfhydril groups and antioxidative potential - FRAP test) in aqueous while one of lipid peroxidation product has increased value (lipid hyperoxide). Aqueous catalase activity in subjects with diabetes and senile cataract is remarkably higher compared with nondiabetic subjects (p<0.0.5). Oxydative stress and antioxidative capacity are well known risk factor in cataractogenesis but in DM 2 patients, oxydative stress is more intensive than in control group.

The increased protein concentration in cerebrospinal fluid is among most prominent biochemical parameter of intensified passage of macromolecules through blood-brain barrier. It is often found in cases of meningeal inflammation, neurodegeneration, neoplastic and traumatic processes developed on brain or spinal cord structures. Protein concentration in cerebrospinal fluid is often determined, but determination of albumin concentrations as well as mathematical models utilizing albumin are more reflective to the pathologic processes on the brain and spinal cord. Our study was limited to the determination of referent values for our laboratory for cerebrospinal fluid albumin concentrations, albumin quotient, as well as albumin transudat and exudat in the function of the age of probands. The results of the study show great agreement with previously published data.

It is obvious that outcome of the cerebral ischemia depends on many of the metabolic reactions that accompany circulatory disturbance, and forcaming neurochemical changes on the cellular level. Cerebral ischemia accompany changes in the neurotransmitters from the group of the biogenic amines, that influence a great deal whole chain of reactions that lead 66 cell to ultimate death. This processes ease up an enables distribution of the cascade reaction in ischemia leisure. To this should be added the fact, that cerebral infarct is followed with selective disturbance on hematoencephal level for 64. monoamines. It is obvious that cerebral infarct involves changes in metabolism of the central neurotransmitters. This changes could have either short or long term consequences on the ischemic process outcome. Therefore our aim in this study was to investigate the influence of the biogenic amines, serotonin and epinephrine as possible markers in estimation of the neural damage, outcome of the ischemic cerebral stroke and clinical presentation throughout correlation in changes of their concentration in liquor. Investigation included 40 patients on hospital treatment on Neurology Clinic of the CHC Pristina. During the follow up study, we estimated changes in concentration levels of the serotonin and epinephrine in liquor throughout different time intervals, correlating to the neurology status, encountering neuroradiology methods CT and MRof the brain, as a criteria in diagnosing acute ischemic cerebral stroke.