Catecholamine contents of different region of adult rat brain are altered following short and long-term exposures to Pb[+2]

Catecholamine is a group of neurotransmitters that is believed to be responsible for the normal function of animal brain. Physiological and behavioral changes of human body have been reported due to the damage of the brain function following lead exposure. Due to the assumption of lead disposal in brain tissue with two year for its half-life, which results in alteration of brain function, we investigated the ability of lead to change the brain catecholamines during short and long-term studies. Rats were exposed daily with varying amounts of lead and catecholamine contents of cerebellum, mid-brain and brain cortex were determined. Acute peritoneal administration of single dose of lead as lead acetate [260 micro mol/Kg] after 2 h reduced [p < 0.05] the catecholamine levels of cerebellum, mid-brain and cortex part by 34.9%, 35.44% and 23.8%, respectively. The extension of experiment time to 5 h, significant [p < 0.05] reductions in catecholamine levels of mentioned regions of brain by 32.35%, 12.35% and 19.3% were seen respectively. Daily intraperitoneal administration of 10 micro mol/Kg lead for 30 and 60 days reduced catecholamines levels of cerebellum [22.22% and 30.44%], midbrain [12.48% and 26.27%] and brain cortex [11.58% and 26.7%] respectively. It might be concluded that brain dysfunction in lead intoxicated rat occurred through the reduction in the catecholamine levels of different parts of brain. Lead might be therefore considered as a probable factor in causing neurological disease in lead exposed man

Comparative effects of copper, iron, vanadium and titanium on low density lipoprotein oxidation in vitro

Oxidation of low density lipoprotein [LDL] has been strongly implicated in the phathogenesis of atherosclerosis. The use of oxidants in dietary food stuff may lead to the production of oxidized LDL and may increase both the development and the progression of atherosclerosis. The present work investigated the effects of some elements including: copper [Cu], iron [Fe], vanadium [V] and titanium [Ti] on in vitro LDL oxidation quantitatively. The first LDL fraction was isolated from fresh plasma by single vertical discontinuous density gradient ultracentrifugation. The formation of conjugated dienes and thiobarbituric acid reactive substances and increase in electrophoretic mobility of LDL were monitored as markers of the oxidation of LDL. It was demonstrated that Cu, Fe, V and Ti exhibited strong oxidant activity in this respect [P<0.001]. Oxidation of LDL in the presence of Cu was more and appeared to be in this order Cu>Fe> V>Ti. Discussion: Cu, Fe, V and Ti are redox-active transition metals that may cause oxidative damage to lipids, proteins and DNA molecules. We suggest that these elements may also influence the oxidation of LDL in vivo, which could increase both the development and progression of atherosclerosis

Spectroscopic studies on titanium ion binding to the apolactoferrin

Titanium [Ti] is a relatively abundant element that has found growing applications in medical science and recently some of Ti compounds are introduced as anticancer drugs. In spite of very limited data which exist on the Ti metabolism, some proteins might be involved in the mechanism of action of Ti. Up to our knowledge, there is not any report in the literature concerning binding of Ti to apolactoferrin. Binding of apolactoferrin with Ti[IV]-citrate was studied by spectroflourimeterey and spectrophotometery techniques under physiological conditions. The spectroflourimeteric studies revealed a significant fluorescence quenching, that indicated binding of apolactoferrin with Ti[IV]. The same reaction was monitored through spectrophotometry technique; this represents a characteristic UV difference band at 267 nm, which is different from lac-Fe [III]. Titration studies show that lactoferrin specifically binds two moles Ti[IV] as complex with citrate per mol protein. Spectroflourimeterey and spectrophotometery techniques indicated that Ti[IV] ions cause a reduction [13%-14%] in binding of Fe[III] to lactoferrin. In overall, we may come to this conclusion that this element might be involved in the iron metabolism

Changes in biochemical parameters related to lipid metabolism following lithium treatment in rat

Lithium is widely used in medicine as an anti-depressive drug. In spite of abundant literature, questions on the side effects of lithium ions are far from being answered. In this study, the effects of lithium on biochemical parameters related to lipid metabolism were investigated. Male Wistar rats were treated with different doses of lithium for a period of up to 60 days. Blood samples were collected and livers were removed for analysis. Lipid related parameters in plasma and livers were measured by st and ard methods. Epididymal fat pads were used to investigate the mechanism of lithium action on lipolysis. It is shown that the major effect of lithium is reduction of HDL-C concentration and the increase of LDL-C only in high doses. Lithium treatment led to a decrease in liver content of triglycerides but phosphohpids increased significantly. Lithium also showed to inhibit lipoprotein lipase activity. This inhibitory effect is potentiated in the presence of citrate. Fat cell lipolysis is also inhibited by lithium, which is not reversed by alpha, and beta-receptor blockers indicating that lithium may exert its effect beyond these receptors. Lithium changes the metabolism of lipoproteins. The finding that lithium decreases HDL and increases LDL concentrations should be considered seriously, especially in patients using this drug for a long period

Changes in catecholamines and acetykholinesterase levels of Cerebellum, mid-brain and brain cortex in chromium treated rats

The short and long term effects of chromium toxicity on brain catecholamines and acetylcholinesterase levels were investigated. Rats were injected daily with varying amounts of chromium. The short term [2 h] administration of chromium [8 mmol/kg] reduced catecholamines level of cerebellum, mid-brain and brain-cortex by 22.8, 19.4 and 21.2% respectively. Acetylcholinesterase activity was also reduced by 36.1, 29.0 and 26.7%. Administration of 38 micro mol/kg chromium for 15, to 60 days, reduced catecholamine levels of cerebellum [8.3-32.8%], midbrain [4.5-20.3%] and brain cortex [6.1-21.3%] respectively. Acetylcholinesterase activity of cerebellum, mid-brain and brain cortex was reduced by 9.4-27.1, 6.8-22.6 and 7.2-24.9 percent respectively. It might be concluded that brain disturbances in chromium treated rat occurred through the reduction in catecholamines and acetylcholinesterase levels

Study of the binding of iron and indium to human serum apo-transferrin

Indium is a heavy metal belonging to group IIIa. It is believed that indium may interfere with iron metabolism from the sites of absorption, transportation, utilization and storage in the cells. The present investigation was established to study and compare the binding of iron and indium to human apo-transferrin [apo-tf]. Pure human apo-tf was used and the binding activity of iron and indium, as a complex with citric acid [1:20], to apo-tf was studied. The binding of iron and indium to apo-tf in Tris-HCl buffer, pH 7.4 showed a maximum absorbance at 465 and 255 nm, respectively. The binding of both metals to apo-tf appears to be pH dependent. Using equilibrium dialysis technique, the binding of iron to apo-tf and the effect of indium on the binding process were also studied. Addition of indium to the outside of dialysis sac reduced iron uptake by 37%. The results indicate that indium competes with iron in binding to apo-tf. Although, the binding sites for these two ions seem to be similar, the binding of iron to apo-tf is more tightly than indium