Marker Of Peroxidation Research Articles

Evaluation of protective action of a-tocopherol in chromium-induced oxidative stress in female reproductive system of rats

The present study was aimed to investigate whether α-tocopherol could protect the chromium (Cr) VI-induced oxidative stress in female reproductive system of rats and to explore the underlying mechanisms of the same. A total of 24 Wistar adult female rats were equally divided into four groups. Group 1 served as control, while groups 2 and 3 were administered K2Cr2O7 (10 mg/kg b.wt. s.c. single dose). In addition to Cr, group 3 also received α-tocopherol @ 125 mg/kg daily by oral gavage for 14 days. Group 4 was maintained as α-tocopherol control (dose as above). Body weights were recorded at the beginning and at the end of experiment. Further, the rats were observed for occurrence of estrus cycle. At the end of 14 days, blood samples were drawn for sero-biochemical analysis. Subsequently, all the rats were sacrificed to collect uterus along with ovaries for assay of tissue peroxidation, anti-oxidant and functional markers, and histopathology. Administration of chromium (Cr) VI to rats revealed a significant (P < 0.05) accumulation of cholesterol and a prolonged diestrus phase leading to impaired fertility in rats. Administration of chromium (Cr) VI significantly (P < 0.05) reduced the antioxidant markers such as superoxide dismutase (SOD) and reduced glutathione (GSH), along with significant (P < 0.05) increase in peroxidation markers such as malondialdehyde and protein carbonyls in ovaries. The functional marker in serum such as total protein was decreased, whereas other functional markers viz alanine transaminase (ALT), blood urea nitrogen (BUN) and creatinine were increased. Prominent pathological changes were observed in the uterus and ovaries of Cr-treated group. Co-treatment with α-tocopherol significantly (P < 0.05) reversed the (Cr) VI induced changes.

A new approach using biomarkers to elucidate the regression state of the invasive alga Caulerpa taxifolia in waters around the Balearic Islands (Western Mediterranean Sea)

Invasive algae alter the structure and function of ecosystems. The green alga Caulerpa taxifolia is an invasive alga introduced in the Mediterranean Sea, whereas Caulerpa prolifera is a native species in Mediterranean waters. The aim of the current work was to determine the oxidative status of both Caulerpa species by means of biomarker measures as a possible indicator of the regression state of C. taxifolia in waters around the Balearic Islands (western Mediterranean Sea). The levels of markers of lipid peroxidation, glutathione concentration, activities of antioxidant enzymes and caulerpenyne production were measured in C. prolifera and C. taxifolia fronds. The concentration of the end product of lipid peroxidation, malondialdehyde, was significantly higher in C. taxifolia than in C. prolifera samples. Antioxidant enzyme activities, namely superoxide dismutase glutathione peroxidase and glutathione reductase, as well as the reduced glutathione : glutathione disulfide ratio were lower in C. taxifolia than in C. prolifera, although the concentrations of malondialdehyde were higher in the alien species. No differences were found in catalase activity or in the concentration of caulerpenyne. In conclusion, the invasive alga C. taxifolia presented a more oxidised status, which could be related to its regression in Mallorcan coastal waters.

Alteration of antioxidant enzymes and oxidative stress in elderly patient.

Reactive oxygen spaces are common by-products of many oxidative biochemical and physiological processes. Therefore the present study was carried out to evaluate the total antioxidant capacity, lipid peroxidation and status of superoxide dismutase in elderly patients with hypertension, Diabetes with hypertension and cardiovascular diseases. Total 85 patients of both sexes were included in the study and further classified into 3 groups as hypertensive, Diabetes with hypertension and cerebrovascular disease/stroke. The 26 healthy subjects who were not on any kind of prescribed medication or dietary restrictions were included in the control group. Malondialdehyde is estimated as a marker of lipid peroxidation, levels were significantly increased in all groups than controls (p

The Impact of Asymmetric Dimethylarginine (ADAMA), the Endogenous Nitric Oxide (NO) Synthase Inhibitor, to the Pathogenesis of Gastric Mucosal Damage

This review was designed to provide an update on the role of asymmetric arginine (ADMA), the endogenous inhibitor of nitric oxide (NO) synthase in the pathophysiology of the upper gastrointestinal (GI) tract. Numerous studies in the past confirmed that NO is a multifunctional endogenous gas molecule involved in most of the body organs' functional and metabolic processes including the regulation of gastrointestinal (GI) secretory functions, motility, maintenance of GI integrity, gastroprotection and ulcer healing. NO is metabolized from L-arginine by enzymatic reaction in the presence of constitutive NO synthase. In upper GI tract, NO acts as a potent vasodilator known to increase gastric mucosa blood flow, regulates the secretion of mucus and bicarbonate, inhibits the gastric secretion and protects the gastric mucosa against the damage induced by a variety of damaging agents and corrosive substances. In contrast, ADMA first time described by Vallance and coworkers in 1992, is synthesized by the hydrolysis of proteins containing methylated arginine amino acids located predominantly within the nucleus of cells. This molecule has been shown to competitively inhibit NO synthase suggesting its regulatory role in the functions of vascular endothelial cells and systemic circulation in humans and experimental animals. Nowadays, ADMA is a potentially important risk factor for coronary artery diseases and a marker of cardiovascular risk. Increased plasma levels of ADMA have been documented in several conditions that are characterized by endothelial dysfunction, including hypertension, hypercholesterolemia, hyperglycemia, renal failure and tobacco exposure. The role of ADMA in other systems including GI-tract has been so far less documented. Nevertheless, ADMA was shown to directly induce oxidative stress and cell apoptosis in gastric mucosal cells in vitro and to contribute to the inflammatory reaction associated with major human pathogen to gastric mucosa, Helicobacter pylori (H.pylori). Infection of gastric mucosa with this germ or H. pylori water extract led to marked increase in the plasma concentration of ADMA and significantly inhibited bicarbonate secretion, considered as one of the important components of upper GI-tract defense system. When administered to rodents, ADMA aggravated gastric mucosal lesions injury induced by cold stress, ethanol and indomethacin and this worsening effect on gastric lesions was accompanied by the significant increase in the plasma level of ADMA. This exaggeration of gastric lesions by ADMA was coincided with the inhibition of NO, the suppression of gastric blood flow and excessive release of proinflammatory cytokine TNF-α. This metabolic analog of L-arginine applied to rats was exposed to water immersion and restraint stress and ischemia-reperfusion, causing an elevation of plasma levels of ADMA and gastric MDA content, which is the marker of lipid peroxidation. These effects, including the rise in the plasma levels of ADMA in rats with stress and ischemia-reperfusion-induced gastric lesions, were attenuated by concomitant treatment with L-arginine, the substrate for NO-synthase, and superoxide dismutase (SOD), a reactive oxygen metabolite scavenger added to ADMA. We conclude that ADMA could be considered as an important factor contributing to the pathogenesis of gastric mucosal damage and inflammatory reaction in H. pylori-infected stomach due to inhibition of NO, suppression of GI microcirculation, and the proinflammatory and proapoptotic actions of this arginine analog.

Influence of MnTE-2-PyP on Inflammation and Lipid Peroxidation in Mouse Asthma Model

Our aim was to investigate the effects of MnTE-2-PyP on some markers of inflammation and lipid peroxidation in mouse asthma model. 24 female mice were divided into four groups: group 1, controls; group 2, injected with ovalbumin (OVA); group 3, treated with MnTE-2-PyP; and group 4, treated with ovalbumin and MnTE-2-PyP. The mice from groups 2 and 4 were injected with 10 μg OVA and 1 mg Imject Alum? in 100 μL phosphate buffered saline (PBS) on days 0 and 14. The animals from groups 1 and 3 were injected with 100 μL PBS + Imject Alum? (1:1). The animals from groups 2 and 4 were subjected to a 30 min aerosol challenge of 1% ovalbumin on days 24, 25 and 26 and those from groups 1 and 3 were subjected to aerosol challenge of PBS at the same time and duration. One hour before inhalation, and 12 hours later the animals from groups 3 and 4 were injected with 100 μL MnTE-2-PyP solution in PBS containing 5 mg/kg. The total cell number, total protein content and 8-isoprostane, IL-4 and IL-5 levels in the bronchialveolar lavage fluid increased in group 2 as compared to the control group. Malone dialdehyde content in the lung homogenate and IgE levels in the serum also increased in this group. The total cell number, total protein content, and levels of 8-isoprostane, IL-4, IL-5 and IgE decreased significantly in group 4 as compared to the OVA group. The parameters set out above in group 3 did not differ significantly from those of the control group. MnTE-2-PyP administered intraperitoneally, 48 hours after the last nebulization, reduced the inflammation and lipid peroxidation in mouse asthma model.

Differential vulnerability of substantia nigra and corpus striatum to oxidative insult induced by reduced dietary levels of essential fatty acids

Oxidative stress (OS) has been implicated in the etiology of certain neurodegenerative disorders. Some of these disorders have been associated with unbalanced levels of essential fatty acids (EFA). The response of certain brain regions to OS, however, is not uniform and a selective vulnerability or resilience can occur. In our previous study on rat brains, we observed that a two-generation EFA dietary restriction reduced the number and size of dopaminergic neurons in the substantia nigra (SN) rostro-dorso-medial. To understand whether OS contributes to this effect, we assessed the status of lipid peroxidation (LP) and anti-oxidant markers in both SN and corpus striatum (CS) of rats submitted to this dietary treatment for one (F1) or two (F2) generations. Wistar rats were raised from conception on control or experimental diets containing adequate or reduced levels of linoleic and α-linolenic fatty acids, respectively. LP was measured using the thiobarbituric acid reaction method (TBARS) and the total superoxide dismutase (t-SOD) and catalase (CAT) enzymatic activities were assessed. The experimental diet significantly reduced the docosahexaenoic acid (DHA) levels of SN phospholipids in the F1 (~28%) and F2 (~50%) groups. In F1 adult animals of the experimental group there was no LP in both SN and CS. Consistently, there was a significant increase in the t-SOD activity (p < 0.01) in both regions. In EF2 young animals, degeneration in dopaminergic and non-dopaminergic neurons and a significant increase in LP (p < 0.01) and decrease in the CAT activity (p < 0.001) were detected in the SN, while no inter-group difference was found for these parameters in the CS. Conversely, a significant increase in t-SOD activity (p < 0.05) was detected in the CS of the experimental group compared to the control. The results show that unbalanced EFA dietary levels reduce the redox balance in the SN and reveal mechanisms of resilience in the CS under this stressful condition.

Altered Antioxidant Status and Increased Lipid Per-Oxidation in Seminal Plasma of Tunisian Infertile Men

Human seminal plasma is a natural reservoir of antioxidants that protect spermatozoa from oxidative damages. There is evidence in literature supports the fact that impairments in seminal antioxidant and lipid per-oxidation status play important roles in the physiopathology of male infertility. Our present study forms the first one which was carried out in Tunisia. We evaluated the antioxidant status in the seminal plasma of 120 infertile men programmed to In Vitro Fertilization (IVF) for the first tentative. Patients were characterized by an idiopathic infertility. They were divided into three groups: normozoospermics who were considered as controls (n=40), asthenozoospermics (Astheno; n=45) and oligoasthenoteratozoospermics (OAT; n=35). Seminal activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) and the levels of glutathione (GSH), zinc (Zn) and malondialdehyde (MDA) were measured. With the significant increase of the seminal activities of SOD and GPX in normozoospermics group, there were positive correlations observed between this enzymes and sperm quality. Also, significant elevated rates of seminal zinc and GSH were observed in control group, but there was contradictory associations reflecting the effects of these antioxidants on semen parameters. However, we noted significant increase of MDA levels in groups with abnormal seminogram. We showed negative associations between this per-oxidative marker and sperm parameters. These results obviously suggested that impairment on seminal antioxidants is an important risk factor for low sperm quality associated to idiopathic infertility and as a result can lead to poor IVF outcome.

Potential role for elevated maternal enzymatic antioxidant status in Andean protection against altitude-associated SGA

Oxidative stress has been implicated in the uteroplacental ischemia characteristic of preeclampsia and small-for-gestational-age (SGA) birth, both of which are more common at high (>2500 m) vs low altitude. Since Andeans are protected relative to Europeans from the altitude-associated rise in SGA, we asked whether alterations in maternal antioxidant status or oxidative stress contributed to their protection. Enzymatic antioxidant (erythrocyte catalase and superoxide dismutase [SOD]) activity and a plasma marker of lipid peroxidation (8-iso-PGF2α) were measured during pregnancy and in the non-pregnant state in Andean or European residents of low (400 m) or high altitude (3600–4100 m). Pregnancy and altitude increased catalase and/or SOD activity to a greater extent in Andeans than Europeans. 8-iso-PGF2α levels were independent of altitude and pregnancy. SOD was lower in mothers of SGA infants at weeks 20 and 36. Our findings are consistent with the possibility that elevated enzymatic antioxidant activity contributes to Andean protection against altitude-associated SGA.

Ffects Of Mntnhex-2-Pyp On Markers Of Inflammation And Lipid Peroxidation In Asthma Mice Model

Background and objective: Iinvestigation of the effects of MnTnHex-2-PyP on some markers of inflammation and lipid peroxidation in an asthma mice model.Methods: The experiment was carried out on 24 female mice C57Bl/6, divided into four groups: group 1, controls; group 2, injected with ovalbumin (OVA); group 3, treated with MnTnHex-2-PyP and group 4, treated with OVA and MnTnHex-2-PyP. The animals from groups 1 and 3 were injected i.p. on days 0 and 14 with a 100 μl phosphate-buffered saline (PBS), and those from groups 2 and 4 were injected with a 100 μl ovalbumin solution, containing 20 μg OVA. On days 24, 25 and 26 the mice from groups 1 and 2 were inhaled with PBS for 30 min, and those from groups 2 and 4 were given a 1% ovalbumin solution. One hour before inhalation, and 12 hours later the animals from groups 1 and 2 were injected i.p. with 100 μl PBS, and those from groups 3 and 4 received a 100 μl MnTnHex-2-Pyp solution in PBS сontaining 0.05mg/kg.Results: Ovalbumin alone (group 2) increased the total cell number, total protein content, the levels of IL-4, IL-5 and 8-isoprostane in bronchoalveolar lavage. Elevations were observed in IgE level in serum, and the malone dialdehyde (MDA) content in the lung homogenate. These markers were decreased significantly in group 4 as compared to the OVA group.Conclusions: MnTnHex-2-Pyp reduces the inflammation and lipid peroxidation in Ovalbumin-induced mice asthma model.

Role of oxidative stress in the pathophysiology of equine laminitis: a comparison of two experimental models

Role of oxidative stress in the pathophysiology of equine laminitis: a comparison of two experimental models

Acute phase response and oxidative stress status in familial Mediterranean fever (FMF)

We aimed to determine acute phase response (APR) and oxidative stress in patients with familial Mediterranean fever (FMF) and compare these characteristics with those in healthy controls; 20 patients with FMF and 15 healthy controls were enrolled in the study. The erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), fibrinogen, and leukocyte levels were determined as markers of APR. Thiobarbituric acid reactive substances (TBARS), conjugated diene, and lipid hydroperoxide levels were measured as markers of lipid peroxidation. Carbonyl group and thiol (T-SH) levels were analyzed to determine the oxidative damage to proteins, and 8-hydroxy-2-deoxyguanosine (8-OHdG) was measured to reflect DNA oxidation. The erythrocyte glutathione (GSH) level, and glutathione peroxidase (GSH-Px), CuZn superoxide dismutase (CuZn SOD), and catalase activities were measured as markers of antioxidant status. Conjugated diene (p < 0.001) and carbonyl group (p < 0.05) levels were significantly higher and GSH-Px activity (p < 0.01) was significantly lower in FMF patients compared with controls. FMF patients in the attack period (n = 8) had significantly higher CRP, ESR, fibrinogen, and leukocyte levels (p < 0.001) than patients in the attack-free period (n = 12). The T-SH level (p < 0.05) was significantly higher and CuZn SOD activity was significantly lower (p < 0.05) in FMF patients in the attack period. The findings revealed upregulated APR during the attack period in FMF patients and enhanced oxidative stress in the FMF patients as compared to controls.

Effects of methotrexate on antioxidant enzyme status in a rodent model

Methotrexate (MTX), a folic acid antagonist is widely used as a cytotoxic chemotherapeutic agent, however its associated hepatotoxicity is considered to be a major clinical side-effect. The aim of this study was to investigate the status of antioxidant enzymes during oxidative stress in liver homogenates of rats subjected to oral methotrexate administration. A total of forty two, 7-week old male Wistar rats with mean weight of 172 g, divided into two groups were used. The first group, control (n = 6), were fed only standard rat chow as their diet and water ad libitum. The second group (n = 36, subdivided into six sub-groups), fed on the same rat chow diet, received orally administered methotrexate at a dose of 13.4 mg/kg at weekly intervals for 6 consecutive weeks. Thiobarbituric acid reactive substance (TBARS) levels and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) were subsequently determined spectrophotometrically on liver homogenates of all animals. It was found that methotrexate caused a significant increase in TBARS levels (an important marker of lipid peroxidation) in the methotrexate administered groups when compared with the control group (P < 0.05). The activities of superoxide dismutase, catalase, and glutathione reductase were significantly decreased in the methotrexate groups at weeks 2, 3, 4, 5 and 6 when compared with the control group (P < 0.05). The results therefore indicate that methotrexate causes oxidative stress by reducing the activities and consequently the effectiveness of the antioxidant enzyme defense system.

Pathological Role of Aminolevulinate in Uremic Patients

Previous reports have demonstrated that δ-aminolevulinate (ALA) can promote iron release from horse spleen ferritin under conditions of high serum ALA levels in uremia; therefore, we speculated that the accumulated ALA in uremic patients would stimulate iron release from ferritin, resulting in accelerated oxidative stress and uremic complications. We measured the plasma ALA of uremic patients and examined the ALA-induced iron release from human ferritin. The participants consisted of 30 hemodialysis patients and 14 healthy subjects. Plasma malondialdehyde was measured as a surrogate marker of lipid peroxidation. The plasma exchange effluent from two patients who had undergone plasma exchange (for the treatment of systemic lupus erythematosus and acute myeloblastic leukemia) was collected and treated to obtain the human ferritin-rich fraction. Iron release from ferritin was examined using bathophenanthroline sulfate. The influence of antioxidants and different pH levels on iron release were investigated. Plasma ALA and malondialdehyde concentration in the hemodialysis patient was significantly higher than that in healthy subjects. ALA was positively correlated with malondialdehyde. The abundance of iron release was dependent on the ALA concentration and incubation time. Iron release at the high pH of 7.6 was decreased compared with that at pH 7.4. Citrate increased iron release at pH 7.4, but citrate-stimulated iron release was totally abolished at pH 7.6. Our study suggests that ALA accumulation may have a role to play in certain complications in uremic patients, such as oxidative stress, by releasing iron from ferritin.

Effect of N-phthaloyl gamma-aminobutyric acid on lipid peroxidation, antioxidants and liver markers in constant light exposed rats

Introduction & Materials and Methods : The effect of N-Phthaloyl GABA on the levels of circulatory lipid peroxidation products such as TBARS (thiobarbituric acid reactive substances), antioxidants: SOD (superoxide dimutase), CAT (catalase), GSH (reduced glutathione), and GPx (glutathione peroxidase), liver markers such as AST (aspartate transaminase), ALT (alanine transaminase), and ALP (alkaline phosphatase), were studied for its protective effect during constant light (LL) exposure in rats. Results: A significant increase in the levels of circulatory TBARS, AST, ALT, and ALP were found in LL exposed rats. These changes were significantly decreased in N-Phthaloyl GABA and LL-exposed rats. The levels of antioxidants were significantly decreased in LL-exposed rats and administration of GABA normalized these changes. Conclusions: Our results indicated that NPhthaloyl GABA offered protection by influencing the levels of the lipid peroxidation products, antioxidants, and liver markers during LL-exposed stress. This might be due to the antistress, anticonvulsant, antinociceptive, and antiulcer activities of N-Phthaloyl GABA. The exact mechanism remains to be explored and further research is needed.

Antioxidant defence and inflammatory response in professional road cyclists during a 4-day competition

Cycling competitions represent an important physical overload even for well-trained individuals. In six professional cyclists, we studied the adaptive oxidative and anti-inflammatory response to a 4-day road cycling competition and its relationship with melatonin, an antioxidant and anti-inflammatory stress hormone. Blood and urine samples were collected before and after the competition. Plasma lipid peroxidation, cytokines (interleukin-1β, interleukin-6, and tumour necrosis factor-α), creatine kinase and other metabolic markers, melatonin, erythrocyte glutathione, and glutathione peroxidase and reductase activities were measured. Urinary excretion of 6-sulphatoxymelatonin was analysed. Lipid peroxidation increased after the competition, but the erythrocyte glutathione pool remained unchanged. Changes in both glutathione peroxidase and reductase activities probably account for the recycling of glutathione after exercise. Interleukin-6 (216%) and tumour necrosis factor-α (159%) but not interleukin-1β increased after exercise. A parallel increase in plasma melatonin concentrations was detected, whereas metabolic markers, including creatine kinase, showed minor modifications. Thus, professional cyclists display an adaptative response to the physical overloads in the competitions for which they are trained. Consequently, they seem to be able to regulate efficiently the intracellular oxidative stress, and prevent an exaggerated pro-inflammatory cytokines induction. A modulator role of melatonin in these adaptive responses is also supported.

Evaluation of &lt;i&gt;in vivo&lt;/i&gt; Antioxidant and Hepatoprotective Activity of &lt;i&gt;Portulaca oleracea&lt;/i&gt; L. against Paracetamol-Induced Liver Toxicity in Male Rats

Problem statement: Oxidative stress plays a major role in paracetamol induced hepatotoxicity. Portulaca oleracea (P.O.) has been shown to exhibit antioxidant properties. The present study aimed to investigate the effect of P.O. on the oxidative stress in Paracetamol-induced hepatic toxicity in male rats. Approach: Forty male rats were divided into four groups. Group I served as control; Group II Received isotonic saline for 20 days and then simultaneously administered with paracetamol 750 mg kg−1 body wt. every 72 h for 10 days; Group III received freshly prepared P.O. for 30 days; Group IV received freshly prepared P.O. for 20 days and then simultaneously administered with paracetamol 750 mg kg−1 body wt. every 72 h for 10 days. All animals were sacrificed cervical decapitation 24 h after the last application and the blood was collected for the determination of serum marker of lipid peroxidation, antioxidant and histology of the liver was performed. Results: Paracetamol treatment resulted in an increase in the hepatic TBARS content and depletion in total antioxidant capacity, reduced glutathione content, catalase and superoxide dismutase activities. Administration of P.O. with paracetamol significantly ameliorated the indices of hepatotoxicity induced by paracetamol. In addition, P.O. alleviated paracetamol induced oxidative changes in liver. Conclusion: The present study demonstrated that P.O. inhibits paracetamol-induced hepatotoxicity and might serve as a protective agent with paracetamol to limit its free radical induced liver injury.

In vitromodel of bone regeneration with bioactive glass and lipid peroxidation

Abstract Tissue regeneration is a complex biological process of vital importance since it allows renewal of damaged cells and organs. The healing of long bones and large joints is often extended or incomplete primarily in elderly people or in polytraumatized patients. Various attempts are made to solve this severe medical and social problem by developing novel bioactive materials, among which bioactive glass is the most attractive because of its osteoconductive and osteostimulative properties. Lipid peroxidation is defined as an important parameter of systematic stress response in patients with traumatic brain injuries and bone fractures. The major bioactive marker and final product of lipid peroxidation, 4-hydroxynonenal (HNE), is a particularly interesting biomolecule because it regulates differentiation, proliferation and apoptosis of cells and might therefore play an important role in regulating the regeneration of damaged tissue such as bone. Therefore, in this study, we investigated the concept of u...

In-vitro and in-vivo antioxidant activity of different extracts of the leaves of Clerodendron colebrookianum Walp in the rat

The in-vitro antioxidant activities of different concentrations of the water, alcoholic, petroleum ether and ethyl acetate extracts of the dried leaves of Clerodendron colebrookianum Walp, and in-vivo antioxidant activity of the water extract was studied in experimental rat models. The results obtained from in-vitro lipid peroxidation induced by FeSO4-ascorbate in rat liver homogenate showed a significant inhibition of lipid peroxidation by different extracts of C. colebrookianum leaf. Water extracts at concentrations (w/v) of 1:30, 1:50, 1:200 and 1:1000 showed the strongest inhibitory activity over the other organic extracts, suggesting maximum antioxidant effect. Chronic feeding of the water extract to Wistar albino rats (both sexes, 150-200 g) in 1 or 2 g kg-1/day doses for 14 days significantly increased the ferric reducing ability of plasma by 19% and 40% on the seventh day, and by 45% and 57% on the fourteenth day of treatment, respectively. Thiobarbituric acid reactive substances (TBARS), as a marker of lipid peroxidation, and some cellular antioxidants (superoxide dismutase, catalase and reduced glutathione) were estimated in heart, liver and kidney. There was a significant reduction in hepatic and renal TBARS with both the doses, without any change in myocardial TBARS. There was no change in the level of antioxidants in heart, liver and kidney, except for the hepatic superoxide dismutase. The findings of this study showed that the leaf extract of C. colebrookianum increased the antioxidant capacity of blood and had an inhibitory effect on the basal level of lipid peroxidation of liver and kidney. This lends scientific support to the therapeutic use of the plant leaves, as claimed by the tribal medicine of North-East India.

Effect of Spinacia oleraceae L. and Perilla frutescens L. on Antioxidants and Lipid Peroxidation in an Intervention Study in Healthy Individuals

Daily consumption of fruits and vegetables is frequently recommended to prevent several diseases. This health-promoting effect is considered to be in part due to the antioxidant content of fruits and vegetables and their ability to decrease oxidative stress. To investigate whether the ingestion of preparations from spinach or perilla, two carotenoid-rich leafy vegetables, is followed by an increase in carotenoid concentration and/or affects parameters of oxidative stress in human blood plasma. 12 healthy volunteers ingested a perilla- or spinach preparation for 10 days (5 mg lutein/d). We quantified antioxidant levels in plasma, kinetics of lipid peroxidation, MDA concentration, and total antioxidative capacity of plasma. We observed a significant increase in lutein content and a moderate increase (n.s.) in beta-carotene content in human blood plasma after consumption of spinach or perilla. The markers of lipid peroxidation tended to decrease, but no influence on antioxidative capacity of plasma could be detected. The high lutein content of perilla caused a more pronounced increase of lutein compared to spinach. Both vegetables seem to be able to influence lipid peroxidation in a beneficial manner.

ECAM: Attacking an Epidemic?

<i>eCAM</i>: Attacking an Epidemic?