Effect of aspartame on biochemical and oxidative stress parameters in rat blood

Aspartame (ASP) is one of the most widely used nonnutritive sweeteners. This study investigates the chronic effects of ASP on hematological and biochemical parameters, and its effects on the oxidative/antioxidative status in the red blood cells of Wistar albino rats. Rats were provided with ASP (40 mg/kg/daily for six weeks) in drinking water. Increased food and fluid intake was observed in the ASP-treated rats. Total body mass was significantly decreased in the ASP-treated rats. Treatment with ASP caused an increase in the concentrations of glucose, cholesterol, LDL-cholesterol, and in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), as well as a decrease in the levels of HDL-cholesterol in the serum. A significant decline in the number of white blood cells (WBC) was observed after ASP uptake. Based on the results we conclude that ASP induces oxidative stress, observed as an alteration of the glutathione redox status, which leads to increased concentrations of nitric oxide (NO) and lipid peroxides (LPO) in the red blood cells. Changes in biochemical parameters, lipid metabolism, as well as changes in the levels of oxidative stress markers and the appearance of signs of liver damage indicate that chronic use of ASP can lead to the development of hyperglycemia, hypercholesterolemia and associated diseases

Glutathione status in the blood of rats after reticulocytosis induced by phenylhydrazine and bleeding

In this experiment, we compared the in vivo effects of phenylhydrazine (PHZ) and bleeding treatment on the redox status and glutathione antioxidative mechanism parameters in the plasma and red blood cells (RBC) of rats. Results showed a lower level of reactive oxygen species (ROS), a higher level of lipid peroxidation and the effective antioxidative role of the glutathione system in the blood of bleeding rats. PHZ-treatment induced higher concentrations of ROS and an accumulation of oxidized glutathione in the plasma, while the glutathione system showed a satisfactory antioxidative capacity in the RBC of rats. When comparing the two anemic groups, the PHZ-treated rats showed marked oxidative stress in the plasma

Copper-induced changes of lipid peroxidation and hemato-biochemical parameters in rat blood: Protective role of flavonoids

The effects of subchronic exposure to copper (Cu) on lipid peroxidation, hemato-biochemical parameters, and the possible protective role of flavonoids Quercetin and (-)-Epicatechin were studied. Male Wistar albino rats were treated with Cu (560 mg/L, p.o. as CuCl2·2H2O for 5 weeks) and Quercetin and (-)-Epicatechin (40 mg/kg BW each, i.p., every third day during the last 3 weeks) alone or in combination. Cu increased the concentration of lipid peroxides, decreased the number of erythrocytes, hemoglobin and hematocrit values and increased the activities of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase. Coadministration of Quercetin and (-)-Epicatechin with Cu lowered the process of lipid peroxidation and restored examined hemato-biochemical parameters to control values. Our results indicate that Cu induced oxidative damage in erythrocytes, which led to anemia, while Quercetin and (-)-Epicatechin showed a protective effect on the hemato-biochemical processes in the blood of rats

Effects of cisplatin on lipid peroxidation and the glutathione redox status in the liver of male rats: The protective role of selenium

The role of oxidative stress in cisplatin (CP) toxicity and its prevention by pretreatment with selenium (Se) was investigated. Male Wistar albino rats were injected with a single dose of cisplatin (7.5 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.) alone or in combination. The results suggest that CP intoxication induces oxidative stress and alters the glutathione redox status: reduced glutathione (GSH), oxidized glutathione (GSSG) and the GSH/GSSG ratio (GSH RI), resulting in increased lipid peroxidation (LPO) in rat liver. The pretreatment with selenium prior to CP treatment showed a protective effect against the toxic influence of CP on peroxidation of the membrane lipids and an altering of the glutathione redox status in the liver of rats. From our results we conclude that selenium functions as a potent antioxidant and suggest that it can control CP-induced hepatotoxicity in rats

Alteration of oxidative stress parameters in red blood cells of rats after chronic in Vivo treatment with cisplatin and selenium

In this study we evaluated the possible protective effects of selenium (Se) on hematological and oxidative stress parameters in rats chronically treated with cisplatin (cisPt). Four groups of Wistar albino rats were examined: a control, untreated rats (I), rats treated with Se (II), rats treated with cisPt (III), and rats treated with Se and cisPt (IV). All animals were treated for 5 days successively and killed 24 h after the last treatment. Hematological and oxidative stress parameters were followed in whole blood and red blood cells (RBC). Results showed that the chronic application of Se was followed by a higher number of reticulocytes and platelets, increased lipid peroxidation and GSH content in the RBC. Cisplatin treatment induced depletion of RBC and platelet numbers and an elevation of the superoxide anion, nitrites and glutathione levels. Se and cisPt co-treatment was followed by an elevation of the hematological parameters and the recovery of the glutathione status when compared to the control and cisPt-treated rats

Neuropeptide Y reduces migration capacity of human choriocarcinoma cell line by altering oxidative/antioxidative status

© TÜBİTAK. Reduced migration capacity of trophoblast cells leads to poor placentation and correlates with severe pregnancy disorders such as intrauterine growth restriction and preeclampsia. Neuropeptide Y (NPY) is sympathetic cotransmitter involved in various physiological processes and its levels are significantly increased in preeclamptic pregnancy compared to healthy pregnancy. In this study the prooxidative role of NPY and its effects on migration capacity of human trophoblast cell line JEG-3 were investigated together with the effects of nitric oxide (NO) depletion, a molecule that was shown to play an important role in promoting cell migration. The cells were treated for 24 h (short-term stimulation) and 72 h (long-term stimulation) respectively with 1 nM NPY. Oxidative/antioxidative status and the migration index of cells were measured. The results showed increased concentrations of oxidative stress parameters (O2•-, H2O2) and molecules of the antioxidant defense system (reduced glutathione and oxidized glutathione), while the levels of intracellular nitrites (indicators of NO) and cell migration index were significantly decreased in trophoblast cells treated with NPY (both at 24 h and 72 h of exposure) compared to the control cells. These results suggest that NPY may significantly contribute to reduced migration capacity of trophoblast cells by generating oxidative stress and reducing the bioavailability of NO

Protective effects of quercetin and Vitamin C against nicotine-induced toxicity in the blood of Wistar rats

© 2016 Institute for Medical Research and Occupational Health. Nicotine is a potential inducer of oxidative stress, through which it can damage numerous biological molecules. The aim of our study was to investigate the prooxidative effects of nicotine and protective (additive or synergistic) effects of quercetin and Vitamin C in the blood of experimental animals, to determine whether the combination of these antioxidants might be beneficial for clinical purposes. Wistar albino rats were receiving intraperitoneal nicotine injection (0.75 mg kg-1 per day) or saline (control group) or nicotine plus quercetin (40 mg kg-1 per day) and Vitamin C (100 mg kg-1 per day) for three consecutive days. On day 4, we determined their blood lipid profile, liver enzymes, oxidative stress parameters, and antioxidative system parameters. Compared to untreated control, nicotine significantly increased total cholesterol, LDLcholesterol, triglycerides, liver enzymes (alanine transaminase, aspartate transaminase, and lactate dehydrogenase) and oxidative stress parameters (superoxide anion, hydrogen peroxide, and lipid peroxide) and decreased HDL-cholesterol, glutathione, and superoxide dismutase/catalase activity. Quercetin + Vitamin C reversed these values significantly compared to the nicotine alone group. Our results confirm that nicotine has significant prooxidative effects that may disrupt the redox balance and show that the quercetin + Vitamin C combination supports antioxidant defence mechanisms with strong haematoprotective activity against nicotine-induced toxicity. In practical terms, this means that a diet rich in Vitamin C and quercetin could prevent nicotine-induced toxicity and could also be useful in the supportive care of people exposed to nicotine

Biotransformation and nitroglycerin-induced effects on antioxidative defense system in rat erythrocytes and reticulocytes

The effects of nitroglycerin (glyceryl trinitrate -GTN) are mediated by liberated nitric oxide (NO) and formed reactive nitrogen species, which induces oxidative stress during biotransformation in red blood cells (RBCs). The aim of this study was to evaluate effects of GTN on antioxidative defense system (AOS) in rat erythrocytes (without) and reticulocytes (with functional mitochondria). Rat erythrocyte and reticulocyte-rich RBC suspensions were aerobically incubated (2 h, 37°C) without (control) or in the presence of different concentrations of GTN (0.1-1.5 mM). After incubation, concentrations of non-enzymatic components of AOS, activities of antioxidative enzymes and oxidative pentose phosphate (OPP) pathway activity were followed in RBC suspensions. In rat reticulocytes, GTN decreased the activity of mitochondrial MnSOD and increased the activity of CuZnSOD. In rat RBCs, GTN induced increase of Vit E concentration (at high doses), but decreased glutathione content and activities of all glutathione-dependent antioxidative enzymes; the OPP pathway activity significantly increased. GTN biotransformation and induction of oxidative stress were followed by general disbalance of antioxidative capacities in both kinds of RBCs. We suggest that oxidative stress, MnSOD inhibition and depletion of glutathione pool in response to GTN treatment lead to decreased bioavailability of NO after GTN biotransformation in rat reticulocytes

Cytotoxic, antimigratory, pro-and antioxidative activities of extracts from medicinal mushrooms on colon cancer cell lines

Methanol extracts of five commercially available mushroom species (Phellinus linteus (Berk. et Curt) Teng, Cordyceps sinensis (Berk.) Sacc., Lentinus edodes (Berk.) Pegler, Coprinus comatus (O. F. Müll.) Pers. and Ganoderma lucidum (Curtis) P. Karst), traditionally used as anticancer agents, were evaluated in vitro for their total phenol and flavonoid contents, cytotoxic and antimigratory activities and antioxidant/prooxidant effects on colon cancer cell lines (HCT-116 and SW-480). Spectrophotometric methods were used for the determination of total phenol content, flavonoid concentrations and DPPH activity of the extracts. Cytotoxic activity was measured by the MTT assay. The antimigratory activity of extracts was determined using the Transwell assay and immunofluorescence staining of ß-catenin. The prooxidant/antioxidant status was followed by measuring the superoxide anion radical (O2•-), nitrite and reduced glutathione (GSH) concentrations. Our results show that the highest phenolic and flavonoid content was found in P. linteus, and its DPPH-scavenging capacity was significantly higher than in other samples. The P. linteus extract significantly decreased cell viability of both tested cancer cell lines. All other extracts selectively inhibited SW-480 cell viability, but did not show significant cytotoxic activity. The mushroom extracts caused changes in the prooxidant/antioxidant status of cells, inducing oxidative stress. All extracts tested on HCT-116 cells demonstrated significant antimigratory effects, which correlated with increased production of O2•- and a reduced level of ß-catenin protein expression, while only P. linteus showed the same effect on SW-480 cells. The results of the present research indicate that the mushroom extracts causes oxidative stress which has a pronounced impact on the migratory status of colon cancer cell lines

Protective effects of oestradiol against cadmium-induced changes in blood parameters and oxidative damage in rats

The aim of this study was to investigate the protective effects of oestradiol (E2, 4 mg kg-1 b.w. i.p.) against cadmium-induced (Cd, 2 mg kg-1 b.w. i.p.) blood changes in rats. Cadmium induced a significant decline in haemoglobin, haematocrit, and total erythrocyte, lymphocyte, and thrombocyte count, whereas total leukocytes and granulocytes increased. A significant increase was also observed in serum cholesterol, triglycerides, glucose, AST, and ALT activities, whereas total protein and albumin levels dropped significantly. Administration of E2 in combination with Cd alleviated most of these adverse effects. In terms of oxidative stress, Cd significantly increased oxygen-free radicals (O2•- and H2O2) in neutrophils and lipid peroxidation in erythrocytes, whereas E2 treatment reversed these changes to control values. Acute Cd poisoning significantly lowered antioxidant enzyme (SOD and CAT) activity and the level of non-enzymatic antioxidants (GSH and vitamin E), while increasing in GSSG. Treatments with E2 reversed Cd-induced effects on the antioxidant defences and significantly lowered Cd-induced oxidative damage in erythrocytes. This study suggests that exogenous E2 effectively restores redox balance in rat erythrocytes and counters adverse haematological and biochemical effects of Cd poisoning. It also improves the antioxidant capacity of erythrocytes, acting in synergy with endogenous antioxidants