The use of comet assay in measuring DNA damage and repair efficiency in child,adult, and old age populations

In the present study, we used the Comet assay to estimate basal DNA damage in three distinct populations aged 5–10, 40–50, and 60–70 years old. The DNA damage induced by hydrogen peroxide and γ-irradiation in the lymphocytes of these populations, as well as their repair activity, was also studied. Finally, we measured apoptosis and necrosis after the effect of these agents. Our results indicate that the older population (60–70 years old) showed higher basal levels of DNA damage and was more sensitive to the effects of the DNA-damaging agents than the adult one (40–50 years old), who, in turn, was more sensitive than the younger population (5–10 years old). A decline of the repair efficiency with age to the DNA damage induced by the two agents was also observed. Apoptosis and necrosis were also affected by age.     

Moderate grade hyperammonemia induced concordant activation of antioxidant enzymes is associated with prevention of oxidative stress in the brain slices

Acute hyperammonemia (HA) induced oxidative stress in the brain is considered to play critical roles in the neuropathology of end stage hepatic encephalopathy (HE). Moderate grade HA led minimal/moderate type HE is more common in the patients with chronic liver failure. However, implication of oxygen free radical ( \textO ₂ ^- {\text{O}}_{ 2}^{ - } ) based oxidative mechanisms remain to be defined during moderate grade HA. This article describes profiles of all the antioxidant enzymes Vis a Vis status of oxidative stress/damage in the brain slices exposed to 0.1–1 mM ammonia, reported to exist in the brain of animals with chronic liver failure and in liver cirrhotic patients. Superoxide dismutase catalyzes the first step of antioxidant mechanism and, with concerted activity of catalase, neutralizes \textO ₂ ^- {\text{O}}_{ 2}^{ - } produced in the cells. Both these enzymes remained unchanged up to 0.2–0.3 mM ammonia, however, with significant increments (P < 0.01–0.001) in the brain slices exposed to 0.5–1 mM ammonia. This was consistent with the similar pattern of production of reactive oxygen species in the brain slices. However, level of lipid peroxidation remained unchanged throughout the ammonia treatment. Synchronized activities of glutathione peroxidase and glutathione reductase regulate the level of glutathione to maintain reducing equivalents in the cells. The activities of both these enzymes also increased significantly in the brain slices exposed to 0.5–1 mM ammonia with concomitant increments in GSH/GSSG ratio and in the levels of total and protein bound thiol. The findings suggest resistance of brain cells from ammonia induced oxidative damage during moderate grade HA due to concordant activations of antioxidant enzymes.     

Ischemia/reperfusion unveils impaired capacity of older adults to restrain oxidative insult

Age independently predicts poor outcome in a variety of medical settings, including sepsis, trauma, severe burns, and surgery. Because these conditions are associated with oxidative stress, we hypothesized that the capacity to constrain oxidative insult diminishes with age, leading to more extensive oxidative damage during trauma. To test this hypothesis, we used suprasystolic inflation of an arm blood pressure cuff to safely induce localized forearm ischemia/reperfusion (I/R) and quantified plasma F₂-isoprostane (IsoP) levels in serial blood samples. Before I/R, IsoP levels were similar in young (20–33 years) and older adults (62–81 years). After I/R challenge, the magnitude and duration of increased IsoP levels was significantly greater in older adults. Because aging is associated with declining levels of sex hormones that contribute to the regulation of antioxidant enzyme expression, we then examined the response to I/R in older women receiving hormone replacement therapy and found that these women did not manifest the amplified IsoP response found in untreated older women. These findings demonstrate that aging impairs the ability to restrain oxidative damage after an acute insult, which may contribute to the increased vulnerability of older adults to traumatic conditions and establishes a useful method to identify effective interventions to ameliorate this deficiency.     

Disparate patterns of age-related changes in lipid peroxidation in long-lived naked mole-rats and shorter-lived mice

A key tenet of the oxidative stress theory of aging is that levels of accrued oxidative damage increase with age. Differences in damage generation and accumulation therefore may underlie the natural variation in species longevity. We compared age-related profiles of whole-organism lipid peroxidation (urinary isoprostanes) and liver lipid damage (malondialdehyde) in long living naked mole-rats [maximum lifespan (MLS) > 28.3 years] and shorter-living CB6F1 hybrid mice (MLS approximately 3.5 years). In addition, we compared age-associated changes in liver non-heme iron to assess how intracellular conditions, which may modulate oxidative processes, are affected by aging. Surprisingly, even at a young age, concentrations of both markers of lipid peroxidation, as well as of iron, were at least twofold (P < 0.005) greater in naked mole tats than in mice. This refutes the hypothesis that prolonged naked mole-rat longevity is due to superior protection against oxidative stress. The age-related profiles of all three parameters were distinctly species specific. Rates of lipid damage generation in mice were maintained throughout adulthood, while accrued damage in old animals was twice that of young mice. In naked mole-rats, urinary isoprostane excretion declined by half with age (P < 0.001), despite increases in tissue iron (P < 0.05). Contrary to the predictions of the oxidative stress theory, lipid damage levels did not change with age in mole-rats. These data suggest that the patterns of age-related changes in levels of markers of oxidative stress are species specific, and that the pronounced longevity of naked mole-rats is independent of oxidative stress parameters.     

Alterations in Antioxidant Enzymes During Aging in Humans

The oxidative stress theory of aging offers the best mechanistic elucidation of the aging phenomenon and other age-related diseases. The susceptibility of an individual depends on the antioxidant status of the body. In humans, the antioxidant system includes a number of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), nonenzymatic antioxidants such as glutathione (GSH), protein –SH, ascorbic acid, and uric acid, and dietary antioxidants. Antioxidant enzymes form the first line of defense against reactive oxygen species. In an earlier report, we showed that the plasma antioxidant potential in humans decreases as a function of age and that there are compensatory mechanisms operating in the body which are induced to maintain the antioxidant capacity during aging. In the present study, we report the relationship between human aging and antioxidant enzymes SOD and CAT; we also correlate the activity of these enzymes with the antioxidant capacity of the plasma. Our results show a significantly higher plasma SOD and CAT activity in older individuals than in younger individuals. The induction in activity of SOD and CAT during human aging may be a compensatory response of the individual to an increased oxidative stress.     

Assessment of the impacts of hydrological fluctuations and salt pans abandonment on Greater flamingos in the Camargue, South of France

Flamingos forage in both commercial salt pans and natural marshes and lagoons along the French Mediterranean coast. In order to assess the impact of changes in management of commercial salt pans and hydrological fluctuations on this flagship species, we evaluated the foraging areas of breeding flamingos using the resightings of 283 breeding flamingos marked with dye at the colony in 1987 and 1989, two years with contrasting hydrological conditions. Teams of observers searched all suitable habitats within 80 km of the colony during the four days following marking and recorded presence of off-duty flamingos. About one-third of the birds were found within 10 km of the colony, but some were seen up to 70 km away. About 24–54% of the birds were found in permanent brackish lagoons and 18–60% in the salt pans, the two most important habitats. In 1989, a dry year with lower water levels in the natural wetlands, the proportion of breeding flamingos using salt pans was twice as high [53%, range (47–60%)] as in 1987 [26%, range (18–29%)], this habitat thus acting as a refuge. Most of the feeding areas shown to be important for flamingos breeding in the Camargue are thus susceptible to variations according to rainfall and to transformations or drying out if the salt pans are abandoned. Our results provide essential benchmarks to reconsider the conservation of this flagship species when management of commercial salt pans changes.     

Is the oxidative stress theory of aging dead?

Currently, the oxidative stress (or free radical) theory of aging is the most popular explanation of how aging occurs at the molecular level. While data from studies in invertebrates (e.g., C. elegans and Drosophila) and rodents show a correlation between increased lifespan and resistance to oxidative stress (and in some cases reduced oxidative damage to macromolecules), direct evidence showing that alterations in oxidative damage/stress play a role in aging are limited to a few studies with transgenic Drosophila that overexpress antioxidant enzymes. Over the past eight years, our laboratory has conducted an exhaustive study on the effect of under- or overexpressing a large number and wide variety of genes coding for antioxidant enzymes. In this review, we present the survival data from these studies together. Because only one (the deletion of the Sod1 gene) of the 18 genetic manipulations we studied had an effect on lifespan, our data calls into serious question the hypothesis that alterations in oxidative damage/stress play a role in the longevity of mice.     

Regulated alterations in redox and energetic status are the key mediators of salinity tolerance in the halophyte <Emphasis Type="Italic">Sesuvium portulacastrum</Emphasis> (L.) L

The present work addresses the importance of antioxidant, redox and energetic parameters in regulating salt-tolerance in Sesuvium portulacastrum. Experiments were conducted on 45 days old plants subjected to 250 and 1,000 mM NaCl stress for 2–8 days. Plants showed no significant change in growth parameters (shoot length, dry weight, and water content) at 250 mM NaCl as compared to control. However, growth of plants was significantly affected at 1,000 mM NaCl. The differential growth behaviour could be attributed to a greater decline in the energetic parameters (in terms of ratios of NADP/NADPH and ATP/ADP) at 1,000 mM NaCl than at 250 mM NaCl. The osmotic stress imposed to plants at 250 mM NaCl was presumably balanced by the accumulation of sodium ions (Na⁺), an energetically favorable process, and did not require an increased synthesis of proline. In contrast, to counter osmotic stress at 1,000 mM NaCl, plants accumulated Na⁺ as well as proline and were, therefore, energetically stressed. Further, the response of enzymatic and molecular antioxidants at 1,000 mM was either close to or even lower than that at 250 mM, which resulted in oxidative damage at 1,000 mM, particularly on longer durations. In conclusion, it is suggested that altered redox and energetic status of the plants could play a key role in mediating the tolerance of Sesuvium under salinity stress.     

Attenuation of Rotenone-Induced Mitochondrial Oxidative Damage and Neurotoxicty in <Emphasis Type="Italic">Drosophila melanogaster</Emphasis> Supplemented with Creatine

Creatine (Cr), an ergogenic nutritional supplement is demonstrated to possess bioenergetic, antiexcitotoxic and antioxidant properties. This study investigated the neuroprotective effects of Cr against rotenone induced oxidative stress, mortality and neurotoxicty in Drosophila melanogaster. We found significant diminution in the endogenous levels of oxidative markers in whole body homogenates of flies exposed to Cr (2–10 mM). Cr supplementation resulted in reduced mortality in flies exposed to rotenone (500 μM) and better performance in a negative geotaxis assay. Further Cr (10 mM) markedly offset rotenone induced mitochondrial oxidative stress, completely restored the GSH levels, nitric oxide levels, activity of Mn-SOD and dopamine depletion. In an oxidative stress bioassay, flies given Cr prophylaxis exhibited marked resistance to paraquat exposure. These data allow us to hypothesize that the neuroprotective action of Cr in Drosophila may be related to its direct antioxidant activity and ability to abrogate rotenone induced mitochondrial oxidative stress.     

Effect of exogenous melatonin on viability, ingestion capacity, and free-radical scavenging in heterophils from young and old ringdoves (Streptopelia risoria)

The decrease of melatonin production with aging contributes to the decline in immune function as organisms age. Treatment with the exogenously administered indoleamine restores the reduced immunological functions. Therefore, we investigated the effect of melatonin on viability, phagocyte ingestion capacity, and free radical generation levels of heterophils from young and old ringdove (Streptopelia risoria) aged 3–4 and 11–13 years, respectively. Animals received a single oral dose of melatonin 1 h before lights off for three consecutive days. Experiments were performed at the acrophases and nadirs of melatonin. Melatonin treatment significantly increased serum melatonin levels at the acrophases, but not at the nadirs of the two age groups. In both young and old animals there was increased heterophil viability at acrophases with respect to nadirs, and also increased cell resistance to oxidative stress in the old animals after the melatonin treatment. At acrophases, the index, percentage and efficiency of phagocytosis all increased significantly, and superoxide anion levels decreased significantly with respect to the nadir values of vehicle and melatonin-treated animals, the effect being greater in young than in old ringdoves. At the nadirs, no change was observed in any parameter analyzed. In both young and old animals, phagocytosis and melatonin were positively correlated, while superoxide anion levels and melatonin were negatively correlated. In conclusion, exogenous melatonin enhanced heterophil viability in old animals as well as increasing phagocytosis and free-radical scavenging in both age groups during the nocturnal period, accompanied by an increase in the levels of the indoleamine.     

Increased Oxidative Damage and Decreased Antioxidant Function in Aging Human Substantia Nigra Compared to Striatum: Implications for Parkinson’s Disease

Parkinson’s disease (PD) is characterized by selective degeneration and loss of dopaminergic neurons in the substantia nigra (SN) of the ventral mid brain leading to dopamine depletion in the striatum. Oxidative stress and mitochondrial damage have been implicated in the death of SN neurons during the evolution of PD. In our previous study on human PD brains, we observed that compared to SN, striatum was significantly protected against oxidative damage and mitochondrial dysfunction. To understand whether brain aging contributes to the vulnerability of midbrain to neurodegeneration in PD compared to striatum, we assessed the status of oxidant and antioxidant markers, glutathione metabolic enzymes, glial fibrillary acidic protein (GFAP) expression and mitochondrial complex I(CI) activity in SN (n = 23) and caudate nucleus (n = 24) during physiological aging in human brains. We observed a significant increase in protein oxidation (P < 0.001), loss of CI activity (P = 0.04) and increased astrocytic proliferation indicated by GFAP expression (P < 0.001) in SN compared to CD with increasing age. These changes were attributed to significant decrease in antioxidant function represented by superoxide dismutase (SOD) (P = 0.03), glutathione (GSH) peroxidase (GPx) (P = 0.02) and GSH reductase (GR) (P = 0.03) and a decreasing trend in total GSH and catalase with increasing age. However, these parameters were relatively unaltered in CD. We propose that SN undergoes extensive oxidative damage, loss of antioxidant and mitochondrial function and increased GFAP expression during physiological aging which might make it more vulnerable to neurotoxic insults thus contributing to selective degeneration during evolution of PD.     

Testing the vicious cycle theory of mitochondrial ROS production: effects of H2O2 and cumene hydroperoxide treatment on heart mitochondria

Vicious cycle theories of aging and oxidative stress propose that ROS produced by the mitochondrial electron transport chain damage the mitochondria leading exponentially to more ROS production and mitochondrial damage. Although this theory is widely discussed in the field of research on aging and oxidative stress, there is little supporting data. Therefore, in order to help clarify to what extent the vicious cycle theory of aging is correct, we have exposed mitochondria in vitro to different concentrations of hydrogen peroxide or cumene-hydroperoxide (0, 30, 100 and 500 μM). We have found that 30 μM hydrogen peroxide (or higher concentrations) inhibit oxygen consumption in state 3 and increase ROS production with pyruvate/malate but not with succinate as substrate, indicating that these effects occur specifically at complex I. Similar levels of cumene-OOH inhibit state 3 respiration with both kinds of substrates, and increase ROS production in both state 4 and state 3 with pyruvate/malate and with succinate. The effects of cumene-OOH on ROS generation are due to action of the peroxide in the complex III or in the complex III plus complex I ROS generators. In all cases, the increase in ROS production occurred at a threshold level of peroxide exposure without further exponential increase in ROS generation. These results are consistent with the idea that ROS production can contribute to increase oxidative stress in old animals, but the results do not fit with a vicious cycle theory in which peroxide generation leads exponentially to more and more ROS production with age.     

Physiology of aging among healthy,older bottlenose dolphins (<Emphasis Type="Italic">Tursiops truncatus</Emphasis>): comparisons with aging humans

Changes in hematological and serum chemistry values have been identified among older compared to younger humans. We hypothesized that healthy bottlenose dolphins (Tursiops truncatus) 30 years and older may demonstrate similar clinicopathological changes with increasing age. Retrospective hematological and serum chemistry data generated from routine, fasted blood samples collected over 10 to 20 years among six healthy dolphins that lived at least 40 years were analyzed to (1) assess linear trends in blood variable values with increasing age, (2) compare mean blood values by older age categories (30–35 years, 36–40 years, and >40 years), and (3) compare the prevalence of clinically high or low blood values by older age categories. Absolute lymphocytes, serum globulins, and mean platelet volume increased linearly with increasing old age. Mean white blood cells, neutrophils, serum globulins, erythrocyte sedimentation rates, serum cholesterol, and serum triglycerides; and the prevalence of neutrophilic leukocytosis, hyperglobulinemia, and hypercholesterolemia, were more likely to be higher as geriatric dolphins got older. A linear decrease in serum albumin with increasing age was present for five of six animals. Serum creatinine decreased among dolphins older than 40 years compared to when they were 30–40 years old. Our study demonstrates that older dolphins have changes in hematological and serum chemistry values similar to those found in older humans. As such, bottlenose dolphins may serve as a useful comparative model for aging in humans. Further studies are needed to assess whether these changes are associated with negative health outcomes and whether targeted therapeutics can help improve quality of life among aging dolphins.     

Loss of adaptation to oxidative stress as a mechanism for aortic damage in aging rats

Cells are armed with a vast repertoire of antioxidant defence mechanisms to prevent the accumulation of oxidative damage. The cellular adaptive response is an important antioxidant mechanism against physiological and pathophysiological oxidative alterations in a cell's microenvironment. The aim of this paper was to study, in the rat aorta, whether this adaptive response and the inflammation associated with oxidative stress were expressed throughout the aging process. We examined the rat aorta, as it is a very sensitive tissue to oxidative stress. Male Wistar rats of 1.5, 3, 12, 18 and 24 months of age were used. Superoxide anion (O2(-)) generation; levels of two antioxidant enzymes, superoxide dismutase (SOD) and catalase; and the levels of prostaglandin E2 (PGE2), an inflammatory marker, were measured. The results for rats at different ages were compared with those for 3 months of age. A balance between production of O2(-) and SOD activity was found in the aorta of rats from 1.5 to 12 months old. Oxidative stress was present in the aorta of old animals (18-24 months), due to a failure in the mechanisms of adaptation to oxidative stress. The observed increase in PGE2 levels in these rats reflected an inflammatory response. All together suggest that vascular oxidative stress and the inflammatory process observed in the old groups of rats could be closely related to vascular aging. Our results also remark the importance of the adaptative response to oxidative stress.     

Oxidative stress and endogenous DNA damage in blood mononuclear cells may predict anti-SARS-CoV-2 antibody titers after vaccination in older adults

Immune senescence in the elderly has been associated with chronic oxidative stress and DNA damage accumulation. Herein we tested the hypothesis that increased endogenous DNA damage and oxidative stress in peripheral blood mononuclear cells of older adults associate with diminished humoral immune response to SARS-CoV-2 vaccination. Increased oxidative stress and DNA double-strand breaks (DSBs) were detected in 9 non-immunocompromised individuals aged 80–96 years compared to 11 adults aged 27–44 years, before, as well as on days 1 and 14 after the first dose, and on day 14 after the second dose of the BNT162B2-mRNA vaccine (all p < 0.05). SARS-CoV-2 vaccination induced a resolvable increase in oxidative stress and DNA damage, but individual DSB-repair efficiency was unaffected by vaccination irrespective of age, confirming vaccination safety. Individual titers of anti-Spike-Receptor Binding Domain (S-RBD)-IgG antibodies, and the neutralizing capacity of circulating anti-SARS-CoV-2 antibodies, measured on day 14 after the second dose in all participants, correlated inversely with the corresponding pre-vaccination endogenous oxidative stress and DSB levels (all p < 0.05). In particular, a strong inverse correlation of individual pre-vaccination DSB levels with both the respective anti-S-RBD-IgG antibodies titers (r = ?0.867) and neutralizing capacity of circulating anti-SARS-CoV-2 antibodies (r = ?0.983) among the 9 older adults was evident. These findings suggest that humoral responses to SARS-CoV-2 vaccination may be weaker when immune cells are under oxidative and/or genomic stress. Whether such measurements may serve as biomarkers of vaccine efficacy in older adults warrants further studies.     

Update on the oxidative stress theory of aging: Does oxidative stress play a role in aging or healthy aging?

The oxidative stress theory of aging predicts that manipulations that alter oxidative stress/damage will alter aging. The gold standard for determining whether aging is altered is life span, i.e., does altering oxidative stress/damage change life span? Mice with genetic manipulations in their antioxidant defense system designed to directly address this prediction have, with few exceptions, shown no change in life span. However, when these transgenic/knockout mice are tested using models that develop various types of age-related pathology, they show alterations in progression and/or severity of pathology as predicted by the oxidative stress theory: increased oxidative stress accelerates pathology and reduced oxidative stress retards pathology. These contradictory observations might mean that (a) oxidative stress plays a very limited, if any, role in aging but a major role in health span and/or (b) the role that oxidative stress plays in aging depends on environment. In environments with minimal stress, as expected under optimal husbandry, oxidative damage plays little role in aging. However, under chronic stress, including pathological phenotypes that diminish optimal health, oxidative stress/damage plays a major role in aging. Under these conditions, enhanced antioxidant defenses exert an “antiaging” action, leading to changes in life span, age-related pathology, and physiological function as predicted by the oxidative stress theory of aging.     

Dietary Vanadium Induces Oxidative Stress in the Intestine of Broilers

The purpose of this study was to examine oxidative stress induced by dietary vanadium in the mucosa of different parts of intestine including duodenum, jejunum, ileum, and cecal tonsil. A total of 420 1-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet or the same basal diet supplemented with 5, 15, 30, 45, and 60 mg/kg vanadium as ammonium metavanadate. During the experimental period of 42 days, oxidative stress parameters were determined for both control and experimental groups. The results showed that malondialdehyde content was significantly higher (p < 0.05 or p < 0.01) in 30, 45, and 60 mg/kg groups than in control group. In contrast, the activities of superoxide dismutase, catalase, and glutathione peroxidase, and ability to inhibit hydroxyl radical, and glutathione hormone content were significantly decreased (p < 0.05 or p < 0.01) mainly in 45 and 60 mg/kg groups in comparison with those of control group. However, the abovementioned oxidative stress parameters were not significantly changed (p > 0.05) in 5 and 15 mg/kg groups. It was concluded that dietary vanadium in excess of 30 mg/kg could cause obvious oxidative stress in the intestinal mucosa, which could impact the antioxidant function of intestinal tract in broilers.     

Lifelong caloric restriction prevents age-induced oxidative stress in the sympathoadrenal system of Fischer 344 x Brown Norway rats

Aging is associated with oxidative damage and an imbalance in redox signaling in a variety of tissues, yet little is known about the extent of age-induced oxidative stress in the sympathoadrenal system. Lifelong caloric restriction has been shown to lower levels of oxidative stress and slow the aging process. Therefore, the aims of this study were twofold: (1) to investigate the effect of aging on oxidative stress in the adrenal medulla and hypothalamus and (2) determine if lifelong 40% caloric restriction (CR) reverses the adverse effects of age-induced oxidative stress in the sympathetic adrenomedullary system. Adult (18 months) and very old (38 months) male Fischer 344 x Brown Norway rats were divided into ad libitum or 40% CR groups and parameters of oxidative stress were analyzed in the adrenal medulla and the hypothalamus. A significant age-dependent increase in lipid peroxidation (+20%, P < 0.05) and tyrosine nitration (+111%, P < 0.001) were observed in the adrenal medulla while age resulted in a reduction in the protein expression of key antioxidant enzymes, CuZnSOD (−27%, P < 0.01) and catalase (−27%, P < 0.05) in the hypothalamus. Lifelong CR completely prevented the age-induced increase in lipid peroxidation in the adrenal medulla and restored the age-related decline in antioxidant enzymes in the hypothalamus. These data indicate that aging results in a significant increase in oxidative stress in the sympathoadrenal system. Importantly, lifelong CR restored the age-related changes in oxidative stress in the adrenal medulla and hypothalamus. Caloric restriction could be a potential non-pharmacological intervention to prevent increased oxidative stress in the sympathetic adrenomedullary system with age.     

Chromium (VI) Can Activate and Impair Antioxidant Defense System

The changes in glutathione-dependent cycle enzymes and catalase activities under Cr(VI)-induced oxidative stress were investigated in two distinct cell lines: L-41−human epithelial-like cells and HLF−fetal human diploid lung fibroblasts, which differ in tissue origin, proliferation, and antioxidant enzymes activities. The chromium concentrations from 1 to 5 μM cause nontoxic effects and activate antioxidant enzymes to overcome oxidative stress. In spite of some differences in the endogenous antioxidant activities, both cell lines reveal the same range of toxic concentrations (20–30 μM). The irreversible inhibition of glutathione-dependent antioxidant enzymes develops under toxic concentrations and serves as a marker of toxicity. The endogenous antioxidant activity influences time-dependent expression of Cr(VI) toxicity and the dynamics of antioxidant enzymes activity under nontoxic conditions. The cell antioxidant defense system is an important marker of the cell adaptive capacity under nontoxic and toxic conditions.     

Evaluation of Oxidative Stress, Antioxidant Status and Serum Vitamin C Levels in Cancer Patients

Taking into account the importance role of lipid peroxidation and antioxidants in the prevention and incidence of cancer, the present study was carried out to determine oxidative stress, serum total antioxidant (TAS), and vitamin C levels in cancer patients. Malondialdehyde(MDA), total antioxidant status, and vitamin C levels of 57cancer patients aged 19–80 years and 22 healthy subjects (control group) aged 22–76 years were evaluated. Serum concentrations of MDA as thiobarbitaric acid complexes were measured by fluorometry method, the serum TAS by using commercial test kits from Randox Laboratories, and vitamin C by using spectrocolorimetric method. The mean serum MDA concentrations of all cancer groups except lung cancer were significantly higher than control group (P < 0.004). The mean total antioxidant status was insignificantly higher than control group. The mean serum vitamin C level was significantly lower in patients as compared to the healthy subjects (PV < 0.0001). In conclusion, an alteration in the lipid peroxidation with concomitant changes in antioxidant defense system in cancer patients may be due to excessive oxidative stress. Serum low levels of vitamin C in the different type of cancer patients in spite of adequate daily intake may be due to increased utilization to scavenge lipid peroxides as well as their sequestration by tumor cells.