Cerium oxide nanoparticles exert antitumor effects and enhance paclitaxel toxicity and activity against breast cancer cells.

Cerium oxide nanoparticles (CeONPs) displayed cytotoxic properties against some cancer cells. However, there is very limited data about the possible antitumoral potential of them in breast cancer cells when used alone and/or together with a chemotherapeutic drug. We investigated the effects of CeONPs alone or in combination with paclitaxel (PAC) on healthy or carcinoma breast cells. After human breast cancer cells (MCF-7) treated with CeONPs alone or together with PAC for 24, 48, and 72 h, the effects of CeONPs on cell viability, apoptosis, migration, and adhesion were investigated. All cell viability and IC50 values of CeONPs and PAC treatments in healthy breast cells (HTERT-HME1) were higher than MCF-7 cells. They showed higher cytotoxicity against MCF-7 cells. CeONPs (10, 20, and 30 mM) and/or abraxane (AB) (2 µM) significantly decreased cell viability values in MCF-7 cells. All CeONPs concentrations increased the number of apoptotic MCF-7 cells. CeONPs (20 and 30 mM) alone or in combination with AB for 72 h treatment also significantly increased the apoptosis in compared to AB alone. CeONPs and/or AB can significantly inhibit the migratory ability of breast cancer cells. The migration rates in co-treated groups with CeONPs and AB were lower than CeONPs treatments. Higher concentrations of CeONPs alone or together with AB inhibited cell adhesion. Our results showed CeONPs can increase cytotoxicity and apoptosis and decrease cell migration and cell adhesion when used alone or together with AB. Therefore, combination of chemotherapeutics with CeONPs may provide a good strategy against cancer.

Whey protein protects liver mitochondrial function against oxidative stress in rats exposed to acrolein.

Acrolein (AC) is one of the most toxic environmental pollutants, often associated with incomplete combustion of petrol, wood, and plastic, oil frying, and tobacco smoking, that causes oxidative damage to DNA and mitochondria. Considering that little is known about the protective effects of whey protein (WP) against AC-induced liver toxicity, the aim of our study was to learn more about them in respect to liver mitochondrial oxidative stress, respiratory enzymes, Krebs cycle enzymes, and adenosine triphosphate (ATP). To do that, we treated Sprague Dawley rats with daily doses of AC alone (5 mg/kg bw in 0.9 % NaCl solution), WP alone (200 mg/kg bw, in 0.9 % NaCl solution), or their combination by oral gavage for six days a week over 30 days. As expected, the AC group showed a drop in glutathione levels and antioxidant, transport chain, and tricarboxylic acid cycle enzyme activities and a significant rise in mitochondrial lipid peroxidation and protein carbonyl levels. Co-treatment with WP mitigated oxidative stress and improved enzyme activities. Judging by the measured parameters, WP reduced AC toxicity by improving bioenergetic mechanisms and eliminating oxidative stress.

Cytotoxic, genotoxic, and carcinogenic effects of acrylamide on human lung cells.

While an association between acrylamide (AC) exposure and the risk of developing cancer has been shown in some studies, there are very limited data on the relationship between AC exposure and lung cancer risk. Thus, we investigated the cytotoxic, genotoxic, and carcinogenic effects of AC on human lung bronchial epithelial cell line (BEAS-2B cells). AC (5 and 10 mM) significantly decreased the cell viability for all treatment times. The comet assay results showed that AC (0.5, 1 and 5 mM) increased the DNA tail (%), tail moment and olive tail moment. By using immunofluorescence, we found that AC (0.5, 1 and 5 mM) induced the formation of both phosphorylated form of the histone H2 variant H2AX (gH2AX) and p53-binding protein 1 (53BP1) foci. AC-treated BEAS-2B cells exhibited various morphological and cytoplasmic changes. The transformed cells can induce form foci and significantly increase the number of colonies in soft agar. We showed for the first time that AC could induce DNA strand breaks, cell transformation, and anchorage-independent growth in BEAS-2B cells. Therefore, AC exposure can induce carcinogenesis in lung cells and may be a risk for lung cancer formation. Further studies are necessary to make a possible risk assessment in humans.

3-Imino derivative-sulfahydantoins: Synthesis, in vitro antibacterial and cytotoxic activities and their DNA interactions.

Sulfahydantoins are five-membered rings found in the structure of chemicals that exhibit antibacterial, anti-inflammatory, and anticonvulsant properties. They also activate serine protease enzymes that catalyze the hydrolysis of peptide bonds. Five 3-imino sulfahydantoin compounds were synthesized by using Strecker synthesis reaction with minor modifications. We used reflux of various aldehydes with excess sulfamide in 85% methanol in the presence of sodium cyanide. The spectroscopic properties of these compounds were studied in detail. Antibacterial activities of all synthesized new compounds against four Gram-positive (Staphylococcus aureus, Bacillus cereus, Bacillus subtilis, Streptococcus mutans) and four Gram-negative (Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, Salmonella Enteritidis) bacteria were investigated by disc diffusion and microdilution method. pBR322 plasmid DNA binding abilities of compounds were investigated in vitro by agarose gel electrophoresis. In addition, the cytotoxic activities of the compounds against the human malignant pleural mesothelioma (SPC212) cell line were determined by the MTT method. The remarkable result in this study is that the synthesized compounds, especially 4b, 4d, and 4e, have significant biological activities. It has been demonstrated that these compounds, which cause DNA damage, also have an important antibacterial effect on both Gram-negative and Gram-positive bacteria when results compared with the control group antibiotics. Compound 4e exhibited the highest antibacterial potency against Streptococcus mutans (24.33 ± 0.57) from Gram-positive bacteria and Pseudomonas aeruginosa (24.66 ± 1.15) from Gram-negative bacteria. At the same time, MTT results determined that compounds 4b, 4d, and 4e showed cytotoxic activity against the SPC212 cells. In particular, compound 4b had a high cytotoxic effect, and the IC50 value was determined as 6.25 µM.

Conjugated linoleic acid protects brain mitochondrial function in acrolein induced male rats.

Acrolein (AC) is a toxic substance that can have a neurotoxic effect. It can cause oxidative stress and mitochondrial dysfunction. Conjugated linoleic acid (CLA), a dietary supplement, has many biological functions. Limited information is available about the effect of CLA on AC-induced brain toxicity. Therefore, the present study aims to investigate the effect of CLA on mitochondrial oxidative stress, respiratory enzymes, krebs cycle enzymes and ATP levels in AC treated rat brain. Sprague Dawley male rats were given AC (5 mg/kg i.p.), CLA (200 mg/kg orally) and CLA with AC for six days per week for 30 days. Some oxidative stress parameters and mitochondrial enzymes such as manganese super oxide dismutase, glutathione peroxidase, NADP+-dependent isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (α-KGDH), malate dehydrogenase, reduced glutathione (GSH), lipid peroxidation (LP), protein carbonyl (PC), oxidative phosphorylation (OXPHOS) and tricarboxylic acid cycle (TCA) enzymes, and ATP levels were determined. AC significantly decreased the activities of GSH, antioxidant enzymes, OXPHOS enzymes (complex I and IV), TCA enzymes (ICDH and α-KGDH) and ATP levels. Significant increases were also observed in mitochondrial LP and PC levels in AC group. Co-treatment with AC + CLA improved oxidative stress and mitochondrial dysfunction caused by AC. As a result of our findings, it was observed that CLA was effective in improving oxidative stress and impaired mitochondrial functions in brain tissue by the effect of AC. Considering the association between neurodegenerative diseases and mitochondrial dysfunction, CLA can play a role in the prevention and therapy of neurodegenerative disorders.

Trimetazidine alone or in combination with gemcitabine and/or abraxane decreased cell viability, migration and ATP levels and induced apoptosis of human pancreatic cells.

BACKGROUND: Trimetazidine (TMZ) is an anti-ischemic agent that can inhibit the fatty acid oxidation. It has been stated that inhibition of fatty acid oxidation may be an acceptable approach to cancer treatment. METHODS: We examined the effects of TMZ alone or together with abraxane (ABX) and/or gemcitabine (GEM) on cell viability, apoptosis, adhesion, migration and ATP levels of human pancreatic cancer cell line PANC-1. RESULTS: TMZ significantly reduced the cell viability at higher concentrations. Lower cell viability values were found in cells co-treated with TMZ + GEM, TMZ + ABX and GEM + ABX. The combined treatment of TMZ with ABX and/or GEM significantly increased the apoptosis rates. The highest percentages of apoptosis were found in TMZ + ABX or TMZ + ABX + GEM treatments. TMZ alone or together with ABX and/or GEM significantly reduced the ATP levels. The lowest migration rates were also found at TMZ + ABX and TMZ + ABX + GEM treatments. CONCLUSIONS: Our study is the first study to indicate that TMZ can induce cytotoxicity and apoptosis and reduce migration and ATP levels, especially in cells co-treated with ABX and/or GEM. A combination strategy based on inhibition of fatty acid oxidation and anticancer drugs may be more effective in the treatment of pancreatic cancers.

Protective effect of Argan oil on mitochondrial function and oxidative stress against acrylamide-induced liver and kidney injury in rats.

CONTEXT: Acrylamide (ACR) is now a risk for general public health. Argan oil (AO) is harvested from the fruits of Argania spinosa and its rich source of antioxidant and phenolic compounds. OBJECTIVE: The aim of present study was to investigate the protective effect of AO against ACR-induced liver and kidney injury in rats. MATERIALS AND METHODS: Rats were exposed to ACR (50 mg/kg/day three times per week), AO (6 ml/kg/day per day) and ACR together with AO for 30 days. Oxidative status and mitochondrial functions were evaluated in liver and kidney. RESULTS: Although ALT, AST, urea and creatine levels in serum, myeloperoxidase and total nitrite (NOx) levels in the tissues, lipid peroxidation and protein carbonyls levels were increased in the ACR-treated rats, cytosolic glucose-6-phosphate dehydrogenase and glutathione-S-transferase activities, mitochondrial antioxidant enzyme activities, glutathione levels, oxidative phosphorylation enzymes, TCA cycle enzymes, mitochondrial metabolic function and ATP level were decreased. The administration of ACR together with AO normalised almost all these parameters. CONCLUSION: Over recent years, compounds that specifically target mitochondria have emerged as promising therapeutic options for patients with hepatic and renal diseases. We think that AO oil is one of these compounds due to its unique content.

Clothianidin induces DNA damage and oxidative stress in bronchial epithelial cells.

Clothianidin (CHN) is a member of the neonicotinoid group of insecticides. Its oxidative and DNA damage potential for human lung cells are not known. Therefore, the present study was designed to examine the effects of CHN on DNA damage and oxidative stress in human bronchial epithelial cells (BEAS-2B) treated with CHN for 24, 72, and 120 hr. Our results indicate that CHN decreased cell viability in a concentration-dependent manner. CHN induced DNA single-strand breaks because alkaline comet parameters such as tail intensity, DNA in the tail, tail moment, and tail length increased. All CHN concentrations also significantly induced the formation of DNA double-strand breaks (DSBs) because it increased phosphorylated H2AX protein foci for all treatment times and p53-binding protein 1 foci for all treatments except for the lowest concentration (0.15 mM) of 120-hr treatment. DNA damage caused by DNA DSBs was not repaired in a 24-hr recovery period. CHN also induced oxidative stress by decreasing reduced glutathione and increasing lipid peroxidation. These results make it necessary to conduct studies about the detailed carcinogenic potential of CHN in humans because it can induce both oxidative and DNA damage.

Cytotoxicity and genotoxicity of clothianidin in human lymphocytes with or without metabolic activation system.

Clothianidin (CHN) is a broad-spectrum neonicotinoid insecticide. Limited studies have been carried out on the cytotoxic and genotoxic effects of both CHN using different genotoxicity tests in human cells with or without human metabolic activation system (S9 mix). Therefore, the aim of this study is to investigate the cytotoxic and genotoxic effects of CHN and its metabolites on human lymphocyte cultures with or without S9 mix using chromosomal aberration (CA) and micronucleus (MN) tests. The cultures were treated with 25, 50, and 100 µg/ml of CHN in the presence (3 h treatment) and absence (48 h treatment) of S9 mix. Dimethyl sulfoxide (DMSO) was used as a solvent control. CHN showed cytotoxic and genotoxic effects due to significant decreases in mitotic index (MI) and nuclear division index (NDI), and significant increases in the CAs, aberrant cells, and MN formation in the absence of S9 mix when compared with solvent control. However, CHN did not significantly induce cytotoxicity and genotoxicity in the presence of S9 mix. Our results indicated that CHN has cytotoxic, cytostatic, and genotoxic potential on human peripheral blood lymphocyte cultures, but not its metabolites under the experimental conditions.

Effects of whey protein and conjugated linoleic acid on acrolein-induced cardiac oxidative stress, mitochondrial dysfunction and dyslipidemia in rats.

Acrolein is a ubiquitous environmental pollutant. Whey protein and conjugated linoleic acid are widely used weight-loss supplements. We aimed to evaluate blood lipid profiles, oxidative stress and mitochondrial bioenergetics function in hearts of rats treated with acrolein and/or the weight-loss supplements. The animals were orally gavaged with acrolein, whey protein, conjugated linoleic acid, acrolein + whey protein or acrolein + conjugated linoleic acid for six days per week during 30 days. Acrolein caused dyslipidemia and oxidative stress in red blood cells and haert mitochondria. Moreover, it caused dysfunction in mitochondrial bioenergetics by decreasing levels of oxidative phosphorylation enzymes, tricarboxylic acid cycle enzymes and ATP. Co-treatment with acrolein + whey protein and acrolein + conjugated linoleic acid ameliorated acrolein-induced oxidative stress and dysfunction in mitochondrial bioenergetics. This amelioration effect was more prominent in acrolein + conjugated linoleic acid group. Interestingly, co-treatment with acrolein + whey protein negatively affected some markers of cardiac injury such as creatinine kinase-MB, lactate dehydrogenase and homocysteine. Conjugated linoleic acid may also cause dyslipidemia because it increased the levels of triacylglycerol, low density lipoproteins and very low density lipoproteins. In conclusion, using some weight loss supplements such as whey protein may adversely affect the biochemical parameters related to cardiovascular system.

Hepatoprotective effects of capsaicin and alpha-tocopherol on mitochondrial function in mice fed a high-fat diet.

Capsaicin (CAP) and alpha-tocopherol (TOC) have antioxidant properties. We investigated effects of CAP and TOC on mitochondrial oxidative stress and mitochondrial bioenergetics in liver of mice fed HFD. AST, ALT, glucose, homeostasis model assessment-insulin resistance index ((HOMA-IR)) and mitochondrial oxidative stress parameters increased, whereas oxidative phosphorylation (OXPHOS) enzymes, tricarboxylic acid cycle (TCA) enzymes, ATP level and mitochondrial metabolic function (MTT) decreased in mice fed a HFD compared to the fed a standard diet (NC). Treatment of HFD together with CAP (HFC group), TOC (HFT group) or TOC and CAP (HCT group) can ameliorate the examined parameters. Because co-treatment with CAP and TOC displayed a better ameliorating effect on liver redox status and mitochondrial bioenergetics functions, they can be useful to protect against HFD and oxidative stress-related in liver diseases.

Acrolein-induced oxidative stress and genotoxicity in rats: protective effects of whey protein and conjugated linoleic acid.

Acrolein (AC), a highly reactive hazardous pollutant, poses serious threats to human health. Whey protein (WP) and conjugated linoleic acid (CLA) have beneficial health implications. We investigated the protective effects of WP and CLA against AC-induced toxicity in rats. The animals were orally gavaged with CLA (200 mg/kg/day), WP (200 mg/kg/day), AC (5 mg/kg/day), CLA + AC (200 + 5 mg/kg/day), and WP + AC (200 + 5 mg/kg/day) six days per week for 30 days. The oral administration of AC significantly induced oxidative stress by increasing thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PCOs) levels and decreasing glutathione (GSH) level in the spleen, thymus, and polymorphonuclear leukocytes (PMNs). It also increased the frequencies of micronucleus (MN) and megakaryocytic emperipolesis (ME) and decreased the ratio of polychromatic erythrocytes (PCEs) in bone marrow. Slight alterations in urinary 8-hydroxydeoxyguanosine (8-OHdG) levels were not significant. Co-treatment with CLA + AC or WP + AC ameliorated the values of oxidative stress, MN, PCE, and ME. These data suggest that CLA and WP can improve the antioxidant defenses and preclude the formation of genetic damage and ME.

Argan oil reduces oxidative stress, genetic damage and emperipolesis in rats treated with acrylamide.

Acrylamide (AA), a well-known toxicant, is present in high-temperature-processed foods in heated foods. Argan oil (AO), a natural vegetable oil, is receiving increasing attention due to its powerful biological properties. However, limited information is available about its effects in lymphoid organs and bone marrow. The aim of this study is to investigate the effects of AO on hematological parameters, 8-hydroxydeoxyguanosine (8-OHdG), thiobarbituric acid reactive substances (TBARs), protein carbonyl (PCO), glutathione (GSH), myeloperoxidase (MPO) levels, the formation of micronucleus (MN) and megakaryocytic emperipolesis (ME) against AA-induced toxicity in rats. The animals were treated with AA (50mg/kg/day), AO (6ml/kg/day per day) and AA+AO (50mg+6ml/kg/day) for 30days. Treatment of rats with AA significantly decreased the hematological parameters, GSH and MPO activity and PCEs ratio while it increased TBARs, PCOs and 8-OHdG levels and formation of MN and ME. No significant differences were observed in the animals received the AO alone. Co-treatment with AA+AO ameliorated almost all of the alterations caused by AA and exhibited protective effect in rats. Based on the obtained results, we suggest that integration of AO in diet or using its supplements may be a good strategy for improving tissue injury in many diseases.

Effects of tartrazine on proliferation and genetic damage in human lymphocytes.

The color additive, tartrazine (TRZ), is widely used in food products, drugs and cosmetics. Genotoxicity of TRZ and its metabolites has not been investigated in detail in the presence and absence of a metabolic activator (S9 mix) in human. Therefore, the aim of this study is to investigate the cytotoxic and genotoxic effects of TRZ and its metabolites on cultured human lymphocytes by using chromosome aberration (CA) and micronucleus (MN) tests. Cultures were treated with 625, 1250 and 2500 µg/ml of TRZ in the presence and absence of S9 mix. TRZ showed cytotoxic activity at the highest concentration due to significant decrease in mitotic index (MI) in the absence of S9 mix when compared with solvent control. TRZ and metabolites significantly increased the CAs and aberrant cells in the presence and absence of S9 mix at the higher concentrations. Increased MN values in cultures with and without S9 mix were found to significantly at the highest concentration when tested. Our results indicated that while both TRZ and its metabolites have genotoxic potential on human lymphocyte cultures with and without S9 mix, TRZ can induce cytotoxicity at the highest concentration in culture without S9 mix under the experimental conditions.

Effects of argan oil on the mitochondrial function, antioxidant system and the activity of NADPH- generating enzymes in acrylamide treated rat brain.

Argan oil (AO) is rich in minor compounds such as polyphenols and tocopherols which are powerful antioxidants. Acrylamide (ACR) has been classified as a neurotoxic agent in animals and humans. Mitochondrial oxidative stress and dysfunction is one of the most probable molecular mechanisms of neurodegenerative diseases. Female Sprague Dawley rats were exposed to ACR (50mg/kg i.p. three times a week), AO (6ml/kg,o.p, per day) or together for 30days. The activities of cytosolic enzymes such as xanthine oxidase (XO), glucose 6-phosphate dehydrogenase (G6PDH), glutathione-S-transferase (GST), mitochondrial oxidative stress, oxidative phosphorylation (OXPHOS) and tricarboxylic acid cycle (TCA) enzymes, mitochondrial metabolic function, adenosine triphosphate (ATP) level and acetylcholinesterase (AChE) activity were assessed in rat brain. Cytosolic and mitochondrial antioxidant enzymes were significantly diminished in the brains of rats treated with ACR compared to those in control. Besides, ACR treatment resulted in a significant reduction in brain ATP level, mitochondrial metabolic function, OXPHOS and TCA enzymes. Administration of AO restored both the cytosolic and mitochondrial oxidative stress by normalizing nicotinamide adenine dinucleotide phosphate (NADPH) generating enzymes. In addition, improved mitochondrial function primarily enhancing nicotinamide adenine dinucleotide (NADH) generated enzymes activities and ATP level in the mitochondria. The reason for AO's obvious beneficial effects in this study may be due to synergistic effects of its different bioactive compounds which is especially effective on mitochondria. Modulation of the brain mitochondrial functions and antioxidant systems by AO may lead to the development of new mitochondria-targeted antioxidants in the future.

Association of brain-derived neurotrophic factor and nerve growth factor gene polymorphisms with susceptibility to migraine.

Migraine is one of the most common neurological diseases worldwide. Migraine pathophysiology is very complex. Genetic factors play a major role in migraine. Neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), play an important role in central nervous system functioning, development, and modulation of pain. This study investigates whether polymorphisms in the BDNF and NGF genes are associated with migraine disease in a Turkish case-control population. Overall, 576 subjects were investigated (288 patients with migraine and 288 healthy controls) for the following polymorphisms: rs6265(G/A), rs8192466(C/T), rs925946(G/T), rs2049046(A/T), and rs12273363(T/C) in the BDNF gene, and rs6330(C/T), rs11466112(C/T), rs11102930(C/A), and rs4839435(G/A) in the NGF gene using 5'-exonuclease allelic discrimination assays. We found no differences in frequency of the analyzed eight polymorphisms between migraine and control groups. However, the frequency of minor A alleles of rs6265 in BDNF gene was borderline significant in the patients compared with the healthy controls (P=0.049; odds ratios [ORs] [95% confidence intervals {CIs}] =0.723 [0.523-0.999]). Moreover, when the migraine patients were divided into two subgroups, migraine with aura (MA) and migraine without aura (MO), the minor TT genotype of rs6330 in NGF was significantly higher in MA patients than in MO patients (P=0.036) or healthy controls (P=0.026), and this disappeared after correction for multiple testing. Also, the rs6330*T minor allele was more common in the MA group than in the MO group or controls (P=0.011, ORs [95% CIs] =1.626 [1.117-2.365] or P=0.007, ORs [95% CIs] =1.610 [1.140-2.274], respectively). In conclusion, this is the first clinical study to evaluate the association between BDNF and NGF polymorphisms in migraine patients compared with health controls. Our findings suggest that the NGF rs6330*T minor allele might be nominated as a risk factor for developing aura in migraine disease. Our results should be considered as preliminary, and they need to be confirmed by future studies.

Oxidative stress and antioxidant defense in patients with chronic hepatitis B.

BACKGROUND: Oxidative stress is defined as a disturbance of balance between free radicals and antioxidant defense system. This study investigated oxidative stress in patients with chronic hepatitis B. METHODS: Sixty nine patients with chronic hepatitis B admitted to the Department of the Infectious Diseases and Clinical Microbiology of Medical Faculty of Ondokuz Mayis University were enrolled into study. Twenty healthy persons were included as a control group. The study group was divided into three groups: healthy controls (group 1), chronic hepatitis B (group 2), and inactive hepatitis B carriers (group 3). Antioxidant status of plasma, including glutathione, glutathione peroxidase, vitamin E, and vitamin C levels were measured. Carbonyl and lipid peroxidation levels were measured as parameters of oxidative stress. RESULTS: Glutathione, glutathione peroxidase, vitamin E, and vitamin C levels were found to be significantly decreased in the chronic hepatitis B group when compared with the control group (9.5 vs. 13.8, p < 0.05; 22.98 vs. 32.4, p < 0.05; 15.1 vs. 16.4, p < 0.05; 12.9 vs. 18.4, p < 0.05, respectively). Carbonyl and lipid peroxidation levels were significantly increased in the chronic hepatitis B group compared to controls (0.7 vs. 0.5, p < 0.05; 2 vs. 0.7, p < 0.05, respectively). However, whereas the glutathione and carbonyl level correlation with HBV DNA levels were mild to moderate (glutathione vs. HBV DNA, r:-0.288, p < 0.05; carbonyl vs. HBV DNA, r:0.317, p < 0.05), the lipid peroxidation levels were strongly related with HBV DNA levels in chronic hepatitis B (r:0.545, p < 0.05). CONCLUSIONS: Oxidative stress was significantly increased in hepatitis B patients. Consequently, decreases were seen at the level of protective antioxidative parameters in the blood of these patients.

Serum prolidase activity and oxidative status in patients with diabetic neuropathy.

We found no data in the literature related to oxidative stress index (OSI), total oxidative status (TOS) and prolidase activity in patients with diabetic neuropathy (DN). In this study, we aimed to evaluate the oxidative status of DN patients via measurement of TOS and serum total antioxidant status (TAS) and estimation of OSI using new automated methods. Thirty-eight healthy participants, 40 diabetic patients without neuropathy, and 39 patients with DN were included. Electrophysiological and neurological examinations were performed. The activity of prolidase and levels of TOS and TAS were determined in the serum of patients. The level of TAS was lower, while the levels of TOS and OSI, and activity of prolidase were higher in both DN and diabetic control groups compared with the healthy subjects (p < 0.05). Prolidase activity was found to be higher in the DN group than in the diabetic control group (p = 0.001). In conclusion, the presence of high TOS and OSI levels together with low levels of TAS in diabetic patients with or without neuropathy may support a role of oxidative stress in the pathogenesis of diabetes mellitus. In addition, increased serum prolidase activity in DN may be interpreted as evidence of increased collagen turnover.

Effect of hexavalent chromium on the growth and physiological and biochemical parameters on Brassica oleracea L. var. acephala DC.

In order to determine the toxic effect of chromium Cr(VI) on the seed germination, the root and shoot length, the root-cotyledonary leaves, the fresh and dry weight in eight-day-old seedlings Brassica oleracea L. var. acephala DC (kale) were treated with various concentrations of Cr in the growth medium. The accumulation of chromium in the tissues was determined in the cotyledons and the roots of the kale seedlings. High rate of Cr uptake was observed in the roots. But the organs could not accumulate large amount Cr. The effect of Cr on B. oleracea var. acephala was evaluated by changes in chlorophyll a, b, lipid peroxidation, proline, ascorbate, protein carbonyl groups, non-protein thiols and peroxidase activity. There were significant decreases in chlorophylls a, b content of the plants treated with Cr. Chromium treated kale seedlings had higher lipid peroxidation and the protein carbonyl groups in cotyledonary leaves than the roots. The changes refer to toxic effects of Cr. There were increases in the non-protein thiol, the total ascorbate, and proline content in the cotyledons and the roots of the seedlings grown on the media containing 0.1 and 0.15 mM Cr. The guaiacol peroxidase activity was higher in the roots of the seedlings than their cotyledons.

Effects of a 900-MHz electromagnetic field on oxidative stress parameters in rat lymphoid organs, polymorphonuclear leukocytes and plasma.

BACKGROUND AND AIMS: The present study investigated the effects of a 900-MHz electromagnetic field (EMF) for 2 h/day for 45 days on lymphoid organs (spleen, thymus, bone marrow), polymorphonuclear leukocytes (PMNs) and plasma of rats, focusing on changes in the enzymatic and nonenzymatic antioxidant system. We determined whether there is any difference between immature and mature rats in terms of oxidative damage caused by EMF and tested recovery groups to determine whether EMF-induced damage is reversible in immature and mature rats. METHODS: Twenty four immature and 24 mature rats were divided randomly and equally into six groups as follows: two control groups, immature (2 weeks old) and mature (10 weeks old); two groups were exposed to 900 MHz (28.2 ± 2.1 V/m) EMF for 2 h/day for 45 days. Two recovery groups were kept for 15 days after EMF exposure. RESULTS: Substantial, deleterious biochemical changes were observed in oxidative stress metabolism after EMF exposure. Antioxidant enzyme activity, glutathione levels in lymphoid organs and the antioxidant capacity of the plasma decreased, but lipid peroxidation and nitric oxide levels in PMNs and plasma and also myeloperoxidase activity in PMNs increased. Oxidative damage was tissue specific and improvements seen after the recovery period were limited, especially in immature rats. CONCLUSIONS: In the present study, much higher levels of irreversible oxidative damage were observed in the major lymphoid organs of immature rats than in mature rats.