Cellular Antioxidant Status Research Articles

Effect of supplementation of tomato juice on the oxidative stress of selected athletes

Background Oxidative stress occurs when there is an imbalance between production and scavenging of free radicals, thus compromising the cellular function and antioxidant status of the body. Athletes, who train competitively, experience more oxidative stress than other average individuals which not only causes damage to cells and DNA, but may also limit aerobic capacity. The present study was conducted to test the effect of tomato juice (lycopene) on the oxidative stress of athletes.

Seasonal differences in the physiology of Carcinus maenas (Crustacea: Decapoda) from estuaries with varying levels of anthropogenic contamination

This study reports the seasonal variability in aspects of the physiology of the shore crab Carcinus maenas from three estuaries in South-west England, each with varying anthropogenic inputs: Avon Estuary (‘relatively low’ impact), Yealm Estuary (‘intermediate’ impact) and Plym Estuary (‘relatively high’ impact). Crabs collected over 12 months from the Avon had a significantly ‘lower’ physiological condition in winter and spring compared to summer and autumn; in particular, haemocyte phagocytic capability (a general indicator of immune function) was significantly higher in winter and spring compared to summer and autumn, and total haemolymph antioxidant status (an indicator of oxidative stress) was significantly lower in winter compared to the remainder of the year. Potentially, shore crabs may be more susceptible to the effects of contaminant exposure, such as increased immunotoxicity (thus, reduction of immune function) and/or oxyradicals (or reactive oxygen species) exposure) especially in seasons of increased susceptibility i.e. summer/autumn (lower phagocytic capability) and winter (lowest antioxidant function). As the Avon was taken to represent the ‘reference’ site, this pattern is considered to reflect the ‘normal’ seasonal variability in shore crab physiology. Shore crab physiological condition from the ‘relatively high’ impact estuary (Plym) revealed increased cellular viability and antioxidant status in autumn and winter compared with that of the ‘standard’ pattern (Avon) However, crabs from the intermediate impact estuary (Yealm) only demonstrated significant physiological differences in summer as shown by a lower cellular viability. All crabs had been exposed to PAHs (confirmed by the presence of PAH metabolites in their urine) which may account for the observed differences in shore crab physiology. In conclusion, to aid understanding of the potential contaminant impacts on biota it is imperative that the ’normal’ seasonal variability of physiological condition be established. Biological effects-based monitoring studies should therefore be employed seasonally to potentially highlight ‘windows of sensitivity’ to contaminant impact.

Strawberry consumption improves plasma antioxidant status and erythrocyte resistance to oxidative haemolysis in humans

Significant increases in the plasma total antioxidant capacity (TAC) have already been reported after acute intake of strawberries. In addition, antihaemolitic effects of strawberry extracts have been recently demonstrated in vitro, revealing that part of the antioxidant properties of strawberry bioactive compounds could lie in their localisation within cell membranes. However, there is a lack of research evidence from in vivo protracted strawberry consumption studies. We carried out a 16-day pilot study where 12 healthy subjects ingested 500g of antioxidants-rich strawberries daily, and we evaluated the potential effects of fruit consumption on biomarkers of plasma and cellular antioxidant status. A significant increase in fasting plasma TAC and in serum vitamin C concentrations were progressively observed during the period of strawberry supplementation. An enhanced resistance to haemolysis was also observed in both AAPH-treated and untreated erythrocytes, collected during and after the period of strawberry consumption. The results obtained in this work suggest that regular consumption of antioxidant-rich strawberries may exert an improvement on the plasma antioxidant status and an increase on the antihaemolitic defenses of human erythrocytes.

Hepatoprotective properties of kombucha tea against TBHP-induced oxidative stress via suppression of mitochondria dependent apoptosis

Kombucha, a fermented tea (KT) is claimed to possess many beneficial properties. Recent studies have suggested that KT prevents paracetamol and carbon tetrachloride-induced hepatotoxicity. We investigated the beneficial role of KT was against tertiary butyl hydroperoxide (TBHP) induced cytotoxicity and cell death in murine hepatocytes. TBHP is a well known reactive oxygen species (ROS) inducer, and it induces oxidative stress in organ pathophysiology. In our experiments, TBHP caused a reduction in cell viability, enhanced the membrane leakage and disturbed the intra-cellular antioxidant machineries while simultaneous treatment of the cells with KT and this ROS inducer maintained membrane integrity and prevented the alterations in the cellular antioxidant status. These findings led us to explore the detailed molecular mechanisms involved in the protective effect of KT. TBHP introduced apoptosis as the primary phenomena of cell death as evidenced by flow cytometric analyses. In addition, ROS generation, changes in the mitochondrial membrane potential, cytochrome c release, activation of caspases (3 and 9) and Apaf-1 were detected confirming involvement of mitochondrial pathway in this pathophysiology. Simultaneous treatment of KT with TBHP, on the other hand, protected the cells against oxidative injury and maintained their normal physiology. In conclusion, KT was found to modulate the oxidative stress induced apoptosis in murine hepatocytes probably due to its antioxidant activity and functioning via mitochondria dependent pathways and could be beneficial against liver diseases, where oxidative stress is known to play a crucial role.

D-serine treatment induces oxidative stress in rat brain

D-serine plays a significant role in neuronal activity, including learning, memory, neuronal migration at developmental stages, and cell-death signaling. It has been also suggested that D-serine can potantiate the neurotoxicity induced by N-methyl-D-aspartate (NMDA) receptor activation due to its coagonist function. However, little is known about the role of D-serine in oxidative stress mechanisms. The aim of this study was to determine the possible neurotoxic or oxidative effects of the dose- (50–200 mg/kg) and time-dependent (2 or 6 hours) D-serine administration on lipid, protein, DNA, mitochondrial integrity (i.e., function), levels of antioxidant enzyme activities (e.g., catalase, glutathione peroxidase, and superoxide dismutase), and glutathione (GSH) in the rat brain. Our results showed that D-serine significantly increases the levels of lipid peroxidation, protein carbonyls, and DNA damage. In addition, D-serine treatment changes cellular antioxidant status due to the decreased levels of antioxidant enzymes, GSH, and mitochondrial function. Therefore, it is concluded that the regulation of D-serine levels in the brain may be an important target for the development of neuroprotective strategies against neurodegenerative processes where excitotoxicity is involved.

Relationship of Cellular Oxidant and Antioxidant Status with Disease Activity in Patients with Rheumatoid Arthritis

Relationship of Cellular Oxidant and Antioxidant Status with Disease Activity in Patients with Rheumatoid Arthritis

Dietary freeze-dried black raspberry's effect on cellular antioxidant status during reflux-induced esophagitis in rats

Introduction Esophageal cancer consists of two distinct types, esophageal adenocarcinoma (EAC) and squamous cell carcinoma, both of which differ significantly in their etiology. Freeze-dried black raspberry (BRB) has been consistent in its ability to modulate the biomarkers and reduce the incidence of carcinogen-induced squamous cell carcinoma in rats. In our previous studies in the esophagoduodenal anastomosis (EDA) model, we have shown that the early modulation of manganese superoxide dismutase (MnSOD) significantly correlates with the development of reflux-induced EAC in rats. In this study we looked at the short-term effects of a BRB-supplemented diet on the modulation of antioxidant enzymes in reflux-induced esophagitis. Methods Male SD rats (8 wk old; n = 3–5) were randomized into three groups---sham-operated, fed control AIN-93M diet (SH-CD), EDA operated and fed either control diet (EDA-CD) or 2.5% (w/w) BRB diet (EDA-BRB). The effect of both reflux and dietary supplementation was analyzed 2 and 4 wk after EDA surgery. Results Animals in the EDA groups had significantly lower weight gain and diet intake compared to SH-CD ( P < 0.05). The sham-operated animals received an average esophagitis score of 0.1 ± 0.1; this increased significantly in EDA-CD animals to 1.8 ± 0.14 ( P < 0.001 versus SH-CD) and in EDA-BRB group to 1.7 ± 0.06 ( P < 0.001 versus SH-CD), with BE changes also present. However, dietary supplementation of BRB did not alter or ameliorate the grade of esophagitis or the induction of BE. BRB diet caused a 43% increase in MnSOD levels compared to EDA-CD (0.73 ± 0.16; P = 0.09); however, this effect was not statistically significant and at 4 wk, EDA-CD (0.58 ± 0.12) showed an increase in MnSOD expression compared to SH-CD (0.34 ± 0.01). Conclusions In conclusion, our data suggest that dietary BRB does not increase the levels of cellular antioxidant enzymes or reduce the levels of lipid peroxidation compared to a control diet, in a short-term study of gastroesophageal reflux induction in the EDA animal model. However, it remains to be tested whether this is indicative of its ineffectiveness to inhibit reflux-induced EAC incidence over the long term.

Protective Effect of Carvacrol on Oxidative Stress and Cellular DNA Damage Induced by UVB Irradiation in Human Peripheral Lymphocytes.

Exposure to ultraviolet B (UVB; 280-320 nm) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of carvacrol on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular an-tioxidant status in human lymphocytes. A series of in vitro assays (hydroxyl radical, superoxide, nitric oxide, DPPH (2,2-Diphenyl-1-picryl hydrazyl), and ABTS (2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging assays) demonstrate antioxidant property of carvacrol in our study. UVB exposure significantly increased thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LHPs), % tail DNA and tail moment; decreased % cell viability and antioxidant status in UVB-irradiated lymphocytes. Treatment with carvacrol 30 min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA, and tail moment and increased % cell viability as carvacrol concentration increased. UVB irradiated lymphocytes with carvacrol alone (at 10 μg/mL) gave no significant change in cell viability, TBARS, LHP, % tail DNA, and tail moment when compared with normal lymphocytes. On the basis of our results, we conclude that carvacrol, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced ROS.

Modulation of oxidative stress by Chlorella vulgaris in streptozotocin (STZ) induced diabetic Sprague-Dawley rats

Chlorella vulgaris (CV), a fresh water alga has been reported to have hypoglycemic effects. However, antioxidant and anti-inflammatory effects of CV in diabetic animals have not been investigated to date. The aim of the present study was to investigate the role of CV in inflammation and oxidative damage in STZ-induced diabetic rats. Male Sprague-Dawley rats (300 - 400g) were divided into 4 groups: control, CV, STZ-induced diabetic rats, and STZ rats treated with CV (150mg/kg body wt). Blood samples were drawn from orbital sinus at 1 and 4 weeks for determination of oxidative cellular damage (DNA damage and lipid peroxidation [malondialdehyde, MDA]), inflammation (tumour necrosis factor alpha, TNF-α) and antioxidant status (catalase, CAT, and superoxide dismutase, SOD). CV did not have any effects on glucose levels in diabetic rats, over the 4 weeks of treatment. However, it reduced significantly DNA damage and blood MDA levels in STZ-induced diabetic rats compared to the control group. Plasma levels of TNF-α however did not show any significant changes in STZ-induced diabetic rats fed with CV. Antioxidant enzyme SOD showed no significant changes in all groups but CAT activity was reduced in STZ-induced diabetic rats compared to the control. CV did not have hypoglycaemic effect but it has a protective role in STZ-induced diabetic rats by reducing oxidative DNA damage, and lipid peroxidation.

Rat Strains Bred for Low and High Aerobic Running Capacity Do Not Differ in Their Survival Time to Hemorrhage

Hemorrhagic shock reflects low tissue perfusion that is inadequate to maintain normal metabolic functions. Often associated with this condition are impairments in cellular oxygen delivery and utilization. Rat strains divergent in their running endurance have been artificially selected over 12 generations. As these rats bred for high (HCR) vs low (LCR) aerobic running capacity have greater tissue O(2) utilization capacity and improved cardiovascular function, we hypothesized that HCR would be more tolerant (i.e., have greater survivability) to the global ischemia of hemorrhagic shock than LCR. To address this hypothesis, survival time to a severe-as substantiated by dramatic changes in plasma lactate, HCO(3), and base deficit-controlled hemorrhage was measured. Male rats were catheterized and, approximately 24 h later, an estimated >35% of the calculated blood volume was removed during a 26-min period while the rats were conscious and unrestrained. Rats were observed for 6 h or until death. Contrary to our hypothesis, survival time in HCR (220 +/- 63 min; n = 6) did not differ statistically (P = 0.46) from that in LCR (279 +/- 53 min; n = 7). Similarly, there were no statistical differences (P >or= 0.08) between rat lines in blood pH, lactate, HCO(3), and base deficit pre- or post-hemorrhage. In addition, few significant differences between lines in response to hemorrhage were detected by measures of cellular antioxidant status in heart, liver, or lung. Since animals with genetically greater tissue oxygen utilization capacity failed to show longer survival times, our results suggest that other mechanisms must play a more dominant role in determining survivability to hemorrhage under conditions of this hemorrhage.

Cellular antioxidant status and human immunodeficiency virus replication.

The factors that stimulate replication of the human immunodeficiency virus (HIV) and determine the period of disease latency are poorly understood. Recent evidence from in vitro cell culture studies of HIV-infected cells suggest that HIV activity is profoundly affected by the presence of antioxidants, such as glutathione and ascorbic acid, in the cell culture medium. These in vitro observations and reports of global glutathione deficiency in nonsymptomatic HIV-seropositive subjects suggest that cellular antioxidant status may be an important factor determining the latency period of HIV infection. The molecular mechanisms underlying HIV activation are beginning to be understood and point to a potentially important role for NK-kappa B, a cellular transcription factor that may be modulated by cellular antioxidant status.

Dietary lipid source alters quercetin effects on antioxidant enzyme/phase I and II gene expression in rat colon

We have demonstrated changes in antioxidant enzyme activities and glutathione metabolism in colonocytes from rats consuming diets containing 0.45% quercetin combined with corn oil or fish oil. The goal of this study was to query whether these changes were regulated at the transcriptional level. Therefore, real‐time PCR was used to assess the relative expression of 15 genes involved in maintaining cellular antioxidant levels and xenobiotic metabolism. Fish oil alone enhanced the level of catalase, and did not affect the expression of any other genes tested. Quercetin decreased the expression of six genes (SOD2, GPx2, GPx4, GLR2, Ephx2, Cyp1a1) and elevated the expression of Ephx1. When the interaction between quercetin and dietary lipid was analyzed, it was noted that quercetin and fish oil tended to lower the expression levels of seven genes, when compared with the fish oil rats not consuming quercetin. However, when quercetin was combined with corn oil, there was a tendency for mixed responses with four genes enhanced and two suppressed. These data suggest that the ability of quercetin to suppress expression of genes involved in regulating cellular antioxidant status and xenobiotic activation/ detoxification is amplified by its combination with fish oil. Funding USDA/CSREES 2005‐34402‐16401, 2007‐118409, and NIEHS P30‐ES09106.

Basal Levels of eIF2α Phosphorylation Determine Cellular Antioxidant Status by Regulating ATF4 and xCT Expression

eIF2alpha is part of a multimeric complex that regulates cap-dependent translation. Phosphorylation of eIF2alpha (phospho-eIF2alpha) is induced by various forms of cell stress, resulting in changes to the proteome of the cell with two diametrically opposed consequences, adaptation to stress or initiation of programmed cell death. In contrast to the robust eIF2alpha phosphorylation seen in response to acute insults, less is known about the functional role of basal levels of eIF2alpha phosphorylation. Here we show that mouse embryonic fibroblasts expressing a nonphosphorylatable eIF2alpha have enhanced sensitivity to diverse toxic insults, including amyloid beta-(1-42) peptide (Abeta), a key factor in the pathogenesis of Alzheimer disease. This correlates with impaired glutathione metabolism because of down-regulation of the light chain, xCT, of the cystine/glutamate antiporter system X(-)(c). The mechanistic link between the absence of phospho-eIF2alpha and xCT expression is nuclear factor ATF4. Consistent with these findings, long term activation of the phospho-eIF2alpha/ATF4/xCT signaling module by the specific eIF2alpha phosphatase inhibitor, salubrinal, induces resistance against oxidative glutamate toxicity in the hippocampal cell line HT22 and primary cortical neurons. Furthermore, in PC12 cells selected for resistance against Abeta, increased activity of the phospho-eIF2alpha/ATF4/xCT module contributes to the resistant phenotype. In wild-type PC12 cells, activation of this module by salubrinal ameliorates the response to Abeta. Furthermore, in human brains, ATF4 and phospho-eIF2alpha levels are tightly correlated and up-regulated in Alzheimer disease, most probably representing an adaptive response against disease-related cellular stress rather than a correlate of neurodegeneration.

Oxidative stress mediated cytotoxicity of cyanide in LLC-MK2 cells and its attenuation by alpha-ketoglutarate and N-acetyl cysteine

Cyanide is a rapidly acting mitochondrial poison that inhibits cellular respiration and energy metabolism leading to histotoxic hypoxia followed by cell death. Cyanide is predominantly a neurotoxin but its toxic manifestations in non-neuronal cells are also documented. This study addresses the oxidative stress mediated cytotoxicity of cyanide in Rhesus monkey kidney epithelial cells (LLC-MK2). Cells were treated with various concentrations of potassium cyanide (KCN) for different time intervals and cytotoxicity was evidenced by increased leakage of intracellular lactate dehydrogenase, mitochondrial dysfunction (MTT assay) and depleted energy status of cells (ATP assay). Cytotoxicity was accompanied by lipid peroxidation indicated by elevated levels of malondialdehyde (MDA), reactive oxygen species (ROS) and reactive nitrogen species (RNS) (DCF-DA staining), diminished cellular antioxidant status (reduced glutathione (GSH), glutathione peroxidase, superoxide dismutase and catalase). These cascading events triggered an apoptotic kind of cell death characterized by oligonucleosomal DNA fragmentation and nuclear fragmentation (Hoechst 33342 staining). Apoptosis was further confirmed by increased caspase-3 activity. Cyanide-induced cytotoxicity, oxidative stress, and DNA fragmentation were prevented by alpha-ketoglutarate (A-KG) and N-acetyl cysteine (NAC). A-KG is a potential cyanide antidote that confers protection by interacting with cyanide to form cyanohydrin complex while NAC is a free radical scavenger and enhances the cellular GSH levels. The study reveals cytotoxicity of cyanide in cells of renal origin and the protective efficacy of A-KG and NAC.

Lipoic Acid Synthase (LASY)

OBJECTIVE—Lipoic acid synthase (LASY) is the enzyme that is involved in the endogenous synthesis of lipoic acid, a potent mitochondrial antioxidant. The aim of this study was to study the role of LASY in type 2 diabetes.RESEARCH DESIGN AND METHODS—We studied expression of LASY in animal models of type 2 diabetes. We also looked at regulation of LASY in vitro under conditions that exist in diabetes. Additionally, we looked at effects of LASY knockdown on cellular antioxidant status, inflammation, mitochondrial function, and insulin-stimulated glucose uptake.RESULTS—LASY expression is significantly reduced in tissues from animal models of diabetes and obesity compared with age- and sex-matched controls. In vitro, LASY mRNA levels were decreased by the proinflammatory cytokine tumor necrosis factor (TNF)-α and high glucose. Downregulation of the LASY gene by RNA interference (RNAi) reduced endogenous levels of lipoic acid, and the activities of critical components of the antioxidant defense network, increasing oxidative stress. Treatment with exogenous lipoic acid compensated for some of these defects. RNAi-mediated downregulation of LASY induced a significant loss of mitochondrial membrane potential and decreased insulin-stimulated glucose uptake in skeletal muscle cells. In endothelial cells, downregulation of LASY aggravated the inflammatory response that manifested as an increase in both basal and TNF-α–induced expression of the proinflammatory cytokine, monocyte chemoattractant protein-1 (MCP-1). Overexpression of the LASY gene ameliorated the inflammatory response.CONCLUSIONS—Deficiency of LASY results in an overall disturbance in the antioxidant defense network, leading to increased inflammation, insulin resistance, and mitochondrial dysfunction.

Effect of ursolic acid, a triterpenoid antioxidant, on ultraviolet-B radiation-induced cytotoxicity, lipid peroxidation and DNA damage in human lymphocytes

Exposure to ultraviolet B (UVB, 280–320) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of ursolic acid on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular antioxidant status in human lymphocytes. Series of in vitro tests (hydroxyl radical, superoxide, nitric oxide, DPPH and ABTS radical scavenging assays) demonstrates antioxidant property of ursolic acid in our study. Treatment of lymphocytes with ursolic acid alone (at 10 μg/mL) gave no significant change in cell viability, thiobarbituric acid reactive substances (TBARSs), lipid hydroperoxides (LHPs), % tail DNA and tail moment when compared with normal lymphocytes. UVB-exposure significantly increased TBARS, LHP and % tail DNA, tail moment; decreased % cell viability and antioxidant status in irradiated lymphocytes. Treatment with ursolic acid 30 min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA and tail moment and increased % cell viability as ursolic acid concentration increased. Based on our results we conclude that ursolic acid, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced reactive oxygen species.

AtNUDT7, a Negative Regulator of Basal Immunity in Arabidopsis, Modulates Two Distinct Defense Response Pathways and Is Involved in Maintaining Redox Homeostasis

Plants have evolved complicated regulatory systems to control immune responses. Both positive and negative signaling pathways interplay to coordinate development of a resistance response with the appropriate amplitude and duration. AtNUDT7, a Nudix domain-containing protein in Arabidopsis (Arabidopsis thaliana) that hydrolyzes nucleotide derivatives, was found to be a negative regulator of the basal defense response, and its loss-of-function mutation results in enhanced resistance to infection by Pseudomonas syringae. The nudt7 mutation does not cause a strong constitutive disease resistance phenotype, but it leads to a heightened defense response, including accelerated activation of defense-related genes that can be triggered by pathogenic and nonpathogenic microorganisms. The nudt7 mutation enhances two distinct defense response pathways: one independent of and the other dependent on NPR1 and salicylic acid accumulation. In vitro enzymatic assays revealed that ADP-ribose and NADH are preferred substrates of NUDT7, and the hydrolysis activity of NUDT7 is essential for its biological function and is sensitive to inhibition by Ca(2+). Further analyses indicate that ADP-ribose is not likely the physiological substrate of NUDT7. However, the nudt7 mutation leads to perturbation of cellular redox homeostasis and a higher level of NADH in pathogen-challenged leaves. The study suggests that the alteration in cellular antioxidant status caused by the nudt7 mutation primes the cells for the amplified defense response and NUDT7 functions to modulate the defense response to prevent excessive stimulation.

Inhibition of Thioredoxin reductase induces apoptosis in neuronal cell lines: Role of glutathione and the MKK4/JNK pathway

The Thioredoxin (Trx)/Thioredoxin reductase (TrxR)-system has emerged as a crucial component of many cellular functions particularly antioxidant defence. We investigated the effect of the selective TrxR inhibitor 1-chloro-2,4-dinitrobenzene (CDNB) on survival and redox status in neuronal cell lines. CDNB was found to cause apoptosis without depletion of glutathione or loss of mitochondrial complex I-activity. Cells treated with CDNB displayed an early increase of reactive oxygen species and rapid activation of stress inducible protein kinases c-Jun N-terminal kinase (JNK) and mitogen activated protein kinase kinase 4 (MKK4). Thus TrxR inhibition by CDNB results in generation of reactive oxygen species and subsequent activation of stress-inducible kinases without impairment of the cellular antioxidant status or mitochondrial function. Inhibition of the specific kinases involved in cell death triggered by Trx/TrxR dysfunction could represent a novel and selective therapeutic approach in neurodegenerative disorders.

Antioxidant to Treat Osteoarthritis: Dream or Reality?

Osteoarthritis is one of the most common chronic diseases that causes pain and physical disability in patient. Although OA is considered as a global disease affecting all joint tissues, cartilage degradation is the end point. The degradation of cartilage results of the combination of mechanical stress and biochemical factors, mainly metalloproteinases and reactive oxygen species (ROS). The activity of reactive oxygen species is balanced by enzymatic and non-enzymatic antioxidants, that act by inhibiting oxidative enzymes, scavenging free radicals or chelating ion metals. Until now, few information is available on the antioxidative status of chondrocytes. Further, the modification of the antioxidative system in osteoarthritis remains unknown. Some antioxidant supplements or drugs with antioxidant properties have been developed to reinforce the cellular antioxidant status. However, until now, there is no consistent evidence that additional antioxidant supply is efficient to relieve OA symptoms or to prevent structural changes in OA cartilage.

Cellular micronutrient deficiency despite normal plasma levels in obese people

It was suggested that part of the increased incidence of cardiovascular disease associated with central adiposity may be caused by a low vitamin E and antioxidant status. To get information on the cellular antioxidant status and on the influence of a weight reduction diet we measured the concentration of vitamin E, vitamin C, ß-carotene and lutein befor and after a 12 week weight reduction diet in 22 adipose volunteers (female, mean BMI 35; BIA fat mean 42,2%) 11 participants underwent a formula weight reduction diet for 8 weeks follewed by a mixed diet for 4 weeks, 11 were treated with an energy reduced mixed diet 12 weeks). At the beginning and at the end of the study blood and buccal mucosa cells were harvested and analysed as recently published. Furthermore routine laboratory investigation including lipids, liver encymes etc ware carried out twice. Vitamin C, E and ß-carotene in buccal mucosa cells and ß-carotene in serum were significantly lower than in healthy normal weigth and age adjusted volunteers. After the 12 week dietary treatment a signifcant increase of Vitamin C (85%), E (77%) and ß-carotene (268%) in buccal mucosa cells and ß-carotene in serum (43%) became evident. In contrast plasma vitamin E did not change reflecting the hepatic controlled transfer to VLDL. The concentration of antioxidants in the buccal mucosa cells were negativly correlated to BMI. The cellular data clearly show that obesity results in a cellular deficiency independent from the diet before weight reduction. Weight reduction however, improves cellular micronutrient conentration. Finally, determination of vitamins in buccal mucosa cells is an easy and non invasive method and gives a much better information on nutritional status than serum levels of vitamins.