فهرست مطالب mohsen ani

Stress may have an important role in the origin and progress of depression and can impair metabolichomeostasis. The one-carbon cycle (1-CC) metabolism and amino acid (AA) profile are some of the consequencesrelated to stress. In this study, we investigated the Paroxetine treatment effect on the plasma metabolite alterationsinduced by forced swim stress-induced depression in mice.

In this experimental study that was carried out in 2021, thirty male NMRI mice (6-8 weeksage, 30 ± 5 g) were divided into five groups: control, sham, paroxetine treatment only (7 mg/kg BW/day), depressioninduction, and Paroxetine+depression. Mice were subjected to a forced swim test (FST) to induce depression and thenwere treated with Paroxetine, for 35 consecutive days. The swimming and immobility times were recorded during theinterventions. Then, animals were sacrificed, plasma was prepared and the concentration of 1-CC factors and twentyAAs was measured by spectrophotometry and high-performance liquid chromatography system (HPLC) techniques.Data were analyzed by SPSS, using One-Way ANOVA and Pearson Correlation, and P<0.05 was considered significant.

Plasma concentrations of phenylalanine, glutamate, aspartate, arginine, ornithine, citrulline, threonine,histidine, and alanine were significantly reduced in the depression group in comparison with the control group.The Homocysteine (Hcy) plasma level was increased in the Paroxetine group which can be associated withhyperhomocysteinemia. Moreover, vitamin B12, phenylalanine, glutamate, ornithine, citrulline, and glycine plasmalevels were significantly reduced in the depression group after Paroxetine treatment.

This study has demonstrated an impairment in the plasma metabolites’ homeostasis in depression andnormal conditions after Paroxetine treatment, although, further studies are required.

High density lipoprotein (HDL) particles are heterogeneous in composition, structure, size, and may differ in conferring protection against cardiovascular disease. HDL associated enzyme, paraoxonase-1 (PON1), has an important role in attenuation of atherogenic low density lipoprotein (LDL) oxidation. The aim of this study was to investigate the associations between HDL particle size and PON1 activity in relation to serum HDL cholesterol (HDL-C) levels. One hundred and forty healthy subjects contributed to this study. HDL was separated by sequential ultracentrifugation and its size was estimated by dynamic light scattering. Paraoxonase activity was measured spectrophotometrically using paraoxon as substrate. Results of this study showed that PON1 activity had negative correlations with HDL mean particle size (r = −0.22, P < 0.01), HDL2/HDL3 ratio, and serum HDL-C levels (r = −0.25, P < 0.01). HDL mean particle size and HDL2/HDL3 ratio had negative correlation with body mass index (BMI), waist hip ratio (WHR), and serum triglyceride (TG) levels, and positive correlation with serum HDL-C levels. Serum HDL-C levels had significant positive correlations with age, total cholesterol (TC), and apolipoprotein A-I (apo A-I) and significant negative correlation with BMI, WHR, and TG. Based on the results of this study, determination of HDL mean particle size beside the serum PON1 activity may help to better understand the CAD risks, pathogenesis, and prognosis, and may also help to design therapeutic protocols toward beneficial modifications of HDL characteristics.

The present experiment was designed to access the effects of Methylmercury chloride (MeHgCl) on antioxidant status, protein concentration, lipid peroxidation and hydroperoxidation in brain parts, spinal cord, lung, heart and pancreas of rats. Twenty male Wistar rats (3 months old) were divided in saline controls (C) and MeHgCl-treated group (MMC). Treated rats were intoxicated with MMC at a dose of 2 mg/kg body weight orally by gavage once a day for 14 consecutive days, for the next 14 days, they were kept intoxicated. Control animals received a corresponding volume of isotonic saline. Health, total feed intake and body weights of rats were monitored daily throughout the study. Both the groups were sacrificed on 29th day. Study revealed an increase in Lipid peroxide (LPO) and Lipid hydroperoxide (LHPO) levels after MeHgCl administration. The levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), total sulfhydryl (TSH) and Protein were significantly declined in all the tissues of MMC treated group as compared to controls. In summary, depletion of antioxidant enzymes in tissues increases MeHgCl accumulation and enhances MeHg-induced oxidative stress, especially LPO and LHPO which plays an important role in tissue degeneration process during MeHgCl intoxication. Results support the hypothesis that depletion of antioxidant enzymes is a primary mechanism of organic mercury toxicity.

Myeloperoxidase (MPO), which is abundantly expressed in neutrophils, catalyzes the formation of a number of reactive oxidant species. However, evidence has emerged that MPO-derived oxidants contribute to tissue damage and initiation and propagation of inflammatory diseases, particularly, cardiovascular diseases. Therefore, studying the regulatory mechanisms of the enzyme activity is of great importance. For clarifying some possible mechanism of the enzyme activity, kinetic investigations of MPO in the presence of Copper (Cu), Cadmium (Cd), and Lead (Pb) ions were carried out in vitro. MPO was partially purified from human white blood cells using ion-exchange and gel-filtration chromatography techniques. Its activity was measured spectrophotometrically by using tetramethyl benzidine (TMB) as substrate. Purified enzyme had a specific activity of 21.7 U/mg protein with a purity index of about 0.71. Cu inhibited MPO activity progressively up to a concentration of 60 mM at which about 80% of inhibition achieved. The inhibition was non-competitive with respect to TMB. An inhibitory constant (Ki) of about 19 mM was calculated from the slope of repot. Cd and Pb did not show any significant inhibitory effect on the enzyme activity. The results of the present study may indicate that there are some places on the enzyme and enzyme-substrate complex for Cu ions. Binding of Cu ionsto these places result in conformational changes of the enzyme and thus, enzyme inhibition. This inhibitory effect of Cu on the enzyme activity might be considered as a regulatory mechanism on MPO activity.

Titanium salts are widely used in pharmacy and industry as intensely white permanent pigment with good covering power in paints, paper, toothpaste, plastics and food dyes. This ion is a redox-active transition metal and may cause oxidative damages to lipids, proteins and DNA molecules. In spite of abundant literature, questions about the side effects of titanium ions still remain to be answered. In this study, the effects of titanium on biochemical parameters related to lipid metabolism were investigated. Male Wistar rats were treated with different doses of titanium for a period of up to 60 days. Blood samples were then collected for analysis. Lipid related parameters in plasma were measured by standard methods. It was shown that titanium reduced plasma VLDL and triglycerides concentrations but increase in LDL-C and cholesterol levels were seen in all experimental groups. Titanium also showed to inhibit lipoprotein lipase activity. The finding that titanium increases LDL and cholesterol concentrations should be considered seriously, especially in people exposing to titanium compounds for a long period.

The potential to cause tissue damage by metal ions is the matter of widespread investigation. Titanium salts are widely used in industry for ceramic painting, in pharmacy for tablet coating and making chemical sunscreens and in medicine as photo catalysts with bactericidal activity. This may address the idea that the exposure to these salts could play a role in metabolic disorders. In this study the effect of Ti on liver contents of lipid fractions was investigated. Male Wistar rats (200-250 g) were used for the experiments. Groups of animals were injected for 10 days with 2.5 mg/kg of titanium chloride, as acute dose and for 30 and 60 days with 0.75 mg/kg as chronic doses. At the end of the experimental period animals were anaesthetized, the abdomens were opened and the livers were perfused with appropriate buffer. Livers were then removed immediately and used fresh or kept frozen until the analysis. Livers were then homogenized and their contents of triglycerides and phospholipids were determined. Blood samples were also collected before killing to measure the lipid levels.Titanium led to a significant increase in phospholipid content of the liver (about 66 %) whereas triglycerides decreased by about 25 to 30 percent in all treated animals. Titanium also reduced plasma free fatty acids and triglycerides significantly but cholesterol and LDL levels were increased in all treated animals. Lipoprotein lipase activity was also inhibited in titanium treated animals.In Conclusion This study is significant because it shows that chronic inhalation or exposure to titanium at workplaces is associated with changes in liver lipid metabolism. Plasma lipid-related parameters were also affected. Although less information is available concerning the mechanism of toxicity but the induction of reactive oxygen species production may be responsible for this effect.

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. Iran. Biomed.

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 standard 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 phospholipids 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. Iran. Biomed.

Insulin resistance syndrome, also referred to as the metabolic syndrome or syndrome X, refers to a constellation of common metabolic and cardiovascular disorders (e.g. obesity, type 2 diabetes mellitus, hypertension, and dyslipidemia), which are all cardiovascular risk factors. Insulin resistance can be induced by fructose-rich diet in rats. We investigated the effect of vanadyl sulfate (0.2 mg/ml in drinking water for 7 days) on glucose, triglyceride, and plasma insulin levels in male Wistar rats that were fed with fructose-rich diets. Control rats were fed with standard chow for 7 days. The animals were divided into three groups: fructose-fed rats, fructose fed-vanadyl sulfate treated rats, and control rats. Fasting plasma glucose levels of the three groups were comparable (p>0.05). Fasting plasma insulin increased in the fructose-fed rats (190 ± 6.3 pM vs. control rats 83.06 ± 3.3 pM, p<0.001), likewise, plasma triglyceride significantly increased in fructose-fed rats (394.0 ± 25.8 vs. control rats 98.63 ± 6.7, p<0001). Vanadyl sulfate treatment prevented the increase in plasma insulin levels in the fructose fed-vanadyl treated rats (78.9 ± 5.1 pM vs. fructose fed-groups, p<0.001). Also vanadyl sulfate treatment significantly decreased plasma triglyceride levels (116.43 ± 6.7 vs. fructose-fed rats, p<0.001). Furthermore, fructose-fed groups had higher fasting insulin resistance index (FIRI: p<0.001) than control rats. In contrast, vanadyl sulfate significantly decreased FIRI in the fructose fed- vanadyl treated groups (p<0.001) compared with fructose- fed animals. These results indicate that administration of low doses of vanadyl sulfate may be advantageous for preservation of the functional characteristics of pancreatic beta cells, probably by improving insulin action and thereby insulin resistance prevention.

The affinity of low density lipoprotein (LDL) to its receptor is very important, because most of LDL-uptake pathway is done by the LDL receptor and the change in size of LDL particle and the modification in its components may affects the LDL affinity for its receptor. In this study, the effects of lipophilic agents such as vitamin E and seven volatile oils: anethol, eugenol, geraniol, limonene, linalool, pulegone and thymol have been investigated on the affinity of LDL to its receptor. LDL receptor was purified of bovine adrenal tissue. LDL was isolated by sequential density ultracentrifugation from normolipidemic human plasma. Then, LDL was labeled with fluoresein isothiocyanate (FITC) at 4°C for 24 h. Native LDL was incubated with various concentrations of each of the volatile oils and vitamin E for 2 h. Finally, the native LDL treated with volatile oils and vitamin E was incubatd with the LDL receptor in the presence of labeled-LDL at 37°C for 30 min. After incubation, the medium was centrifuged at 4000 ×g for 20 min and the fluorescence intensity (FI) of supernatant from each sample was determined at excitation 495 nm and emission 515 nm. The elevation of FI in each fraction demonstrates increasing the affinity of non-labeled-LDL to its receptor. We showed that vitamin E and volatile oils increased the affinity of LDL to its receptor, and among these compounds, vitamin E and thymol are the best agents that increase the affinity of native LDL to its receptor. The effects of these compounds are as follows: vitamin E > thymol > eugenol > anethol > geraniol > linalool > limonene > pulegone. These findings raise the possibility that vitamin E and some of the volatile oils may decrease the effect of LDL in formation of atherosclerotic lesions.

There are many reports for involvement of ATP-sensitive potassium channels in pancreatic, cardiac and vascular smooth muscle cells. This study examined the effect of single doses of K+ channel openers; diazoxide, minoxidil and K+ channel blockers; chlorpropamide, glibenclamide on serum concentration of aldosterone in male rats. Blood samples were obtained 60 minutes after drug treatment and serum aldosterone level was determined by RIA. The basal serum aldosterone was 659.32 ± 71.48 pg/ml and after diazoxide or minoxidil administration increased to 1188.53 ± 99.45 pg/ml and 1392.69 ± 177.83 pg/ml, respectively. Chlorpropamide or glibenclamide treatment did not produce any change in basal serum aldosterone concentration, but in early streptozotocin-induced diabetic rats decreased serum aldosterone level significantly (P<0.001). Pretreatment with glibenclamide blocked aldosterone response to diazoxide but did not affect aldosterone response to exogenous ACTH to the same extent. Effect of diazoxide in insulin-treated rats was approximately similar to that of normal rats. Comparison of blood glucose concentration determined in normal, insulin treated and diabetic rats after different drug administration showed that there is no correlation between blood glucose level and the responses observed in serum hormone concentration. The results indicate that regulatory processes involved in the secretion of aldosterone are responsive to drugs affecting glibenclamide–sensitive K+ channels