Effects Of Antioxidant Vitamins Research Articles

Circulating Levels of Vitamins A, C, and E-Alpha in Organ Donors After the Neurologic Determination of Death.

The antioxidant effects of vitamins may attenuate the oxidative stress on organs imposed by ischemia-reperfusion injury during the process of organ transplantation from brain-dead donors. Circulating levels of vitamins A, C, and E-α in donors after brain death and their relationships to donor demographics, management, organ utilization, and recipient outcomes are largely unknown. An observational, prospective, cohort study of 84 consecutive brain-dead organ donors managed at a single organ procurement recovery center was conducted. Vitamin levels were drawn immediately prior to procurement. Levels of serum vitamins A and E-α and plasma vitamin C were below normal in 80%, 85%, and 92% of donors and deficient in 40%, 62%, and 63%, respectively. Vitamin C deficiency was associated with a longer time between death and specimen collection (P = .004). Death from head trauma and stroke were associated with lower levels of vitamin A than from anoxic causes (P = .003) and smokers had greater vitamin C deficiency (P = .03). During donor management, vitamin C deficiency was associated with longer vasopressor support (P = .03) and normal levels of vitamin E-α were associated with reaching a lower alanine transferase compared to those with subnormal levels (P < .05). Donors deficient in vitamin E-α were less likely to have a liver recovered for transplantation (P = .005). Vitamin levels were not associated with the recipient outcomes examined. Circulating vitamins A, C, and E-α is profoundly low in brain-dead organ donors, associated with relevant demographic features of the donor, and may influence donor management and organ utilization.

Antioxidant Effects of Vitamin C on Some Hematological Parameters of Male Wistar Rats Exposed to Lead Acetate

The study investigated the effects of vitamin C on platelet parameters, white blood cell count and white blood cells differentials in Wistar rats exposed to lead acetate. A total of twenty-four male Wistar rats weighing between 160g and 200g were utilized. The experimental animals were divided into four groups of six rats each (n=6). Group 1 served as the control group (received normal feed and water), group II received 10mg/kg body weight of lead acetate, group III received 100mg/kg body weight of Vitamin C, and group IV received 10mg/kg body weight of lead acetate followed by 100mg/kg body weight of Vitamin C. Lead and Vitamin C, along with normal feed, were administered for four weeks. Blood samples were collected via jugular puncture and stored in EDTA bottles for analysis to determine the blood profile of the rats. The results showed significant increase in Platelet Count (PLT) in group III and a significant decrease in Mean Platelet Volume (MPV) in group IV (Pb + vitamin C). The Mean Platelet Width (MPW) showed decrease in groups 2, 3, and 4 compared to the control group, although this decrease was not statistically significant. The study also noted an elevated level of white blood cells (WBC) in response to the antioxidant treatment, indicating a potential positive impact on immune function. In conclusion, this study demonstrates the therapeutic effect of Vitamin C against the toxic effects of lead on platelet parameters and white blood cell count and differentials.

Antioxidative effects of vitamin D in muscle dysfunction

Graphical abstract Abstract Pathological conditions characterized by systemic inflammation and oxidative stress can often impair the muscle cells efficiency. The gradual decline of muscle mass and tone drastically reduces the motor skills of the patient affecting the simplest daily activities. Muscle dysfunction, resulting in the deterioration of muscle tissue, can lead to a serious situation of muscle wasting that can evolve into sarcopenia. In addition, muscle dysfunction causing metabolic disorders impairs the quality of life. The function of skeletal muscle is deeply conditioned by environmental, nutritional, physical, and genetic factors. Proper nutrition with balanced protein and vitamins intake and an active lifestyle helps to strengthen tissues and counteract pathological conditions and generalized weakness. Vitamin D performs antioxidant actions, indispensable in skeletal muscle. Epidemiological data indicate that vitamin D deficiency is a widespread status in the world. Vitamin D deficiency induces mitochondrial failure, reduced production of adenosine triphosphate, oxidative injury, and compromised muscle function. Among the different types of antioxidants, vitamin D has been identified as the main compound that can improve the effectiveness of the treatment for muscle weakness and improve conditions related to sarcopenia. The purpose of this review is to analyze molecular processes used by vitamin D against oxidative stress and how it can affect muscle function in order to assess whether its use as a supplement in inflammatory pathologies and oxidative stress can be useful to prevent deterioration and improve/maintain muscle function.

Vitamin E Prevented Hepatic and Renal Tissue Damage in Hypothyroid Rats.

Considering antioxidant effects of vitamin E (Vit E), in the present study, the effect of Vit E on liver and kidney functions and oxidative stress parameters in tissues of these organs of hypothyroid (Hypo) rats were reported. The animals were included in three groups:(1) control, (2) hypo, and (3) hypo-hypo-Vit E. Hypothyroidism was induced in rats by giving 0.05% propylthiouracil (PTU) in drinking water. Besides PTU, the rats in group 3 were daily injected with Vit E (20 mg/kg) for 42 days. The animals were deeply anesthetized and sacrificed, and the serum of the rats was immediately removed to measure thyroxin level and subsequent analysis. The liver and kidney tissues were also immediately removed for biochemical oxidative stress criteria. PTU administration reduced serum thyroxin level and also thiol content, superoxide dismutase (SOD), and catalase (CAT) activities in the liver and kidney tissues while increasing malondialdehyde (MDA). Hypothyroidism also increased alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine while decreasing albumin. Vit E increased thiol, SOD, and CAT in the liver and kidney tissues while diminished MDA. Vit E also decreased ALT, BUN, and creatinine while increased albumin. The results of this study showed that Vit E prevented liver and renal tissue damage in hypothyroid rats.

Antioxidant Effect of Vitamins in High-intensity Cross-country Running and the Effect of Physical Strength Supplement

Antioxidant Effect of Vitamins in High-intensity Cross-country Running and the Effect of Physical Strength Supplement

Anticholinesterase activity and Antioxidant Effect of Vitamin E in Aluminum Chloride Induced Toxicity in Drosophila Melanogaster

BackgroundAluminum chloride (AlCl3) has been used to model neurotoxicity and Alzheimer’s disease (AD) like neurodegeneration in various animal models (Bondy, 2010). AlCl3 toxicity has been reported to be associated with impaired locomotor performance, learning, memory, oxidative stress and cholinergic impairment which are features seen in AD patients (Ribes et al., 2008). AlCl3acts as a cholinotoxin (Gulya et al., 1990) and cause alterations on the cholinergic activity, a key event in the neurochemistry of AD (Rakonczay et al., 2005). Reduced cholinergic function in the brain has been shown to result in memory impairment in AD (Mukherjee et al., 2007). The use of compounds to inhibit acetylcholinesterase (AChE) activity (to reduce the hydrolysis of acetylcholine) has been a therapeutic approach in managing AD (Taylor and Radić 1994). Vitamin E has been proposed as a potential clinical intervention for AD given its antioxidant and anti‐inflammatory characteristics. However, there are very few studies on its anticholinesterase activity and there also controversies as to whether vitamin E is beneficial in AD. We therefore evaluated the anticholinesterase and antioxidant activity of vitamin E in aluminium chloride induced toxicity in Drosophila melanogaster.MethodsD. melanogaster (Harwich strain, 3‐5 days) were utilized for this study. In order to determine the appropriate dose of vitamin E to be utilized for this study, a 15 days survival study (where mortality rate was recorded daily) was carried out with varying dose of Vitamin E (2.5mg and 5mg). Subsequently, 2.5mg of vitamin E produced the least mortality of flies and was utilized for this study. The choice of concentration for AlCl3was based on previous studies on aluminum toxicity in D. melanogaster [Wu et al., 2012; Ogunsuyi, 2020]. Flies (both genders) were divided into 4 groups with 50 flies per vial. Group I served as control and were reared on their cornmeal diet while group II were treated with 40mM aluminum chloride (AlCl3) via their diet. Group III flies were fed with normal diet containing 2.5mg of vitamin E while Group IV were co‐administered with 40 mM AlCl3and 2.5mg of vitamin E via their diet. The flies were maintained on these treatments at room temperature for seven (7) days. All experiments were carried out in five replicates (n=5). Negative geotaxis was carried out to assess for locomotion deficit. At the end of the experimental period, the flies were homogenized and the supernatant were used to assay for AchE activity, malonaldehyde (MDA) concentration, superoxide dismutase (SOD), catalase (CAT) and glutathione S‐transferase (GST) activities.ResultsAlCl3induced toxicity reduced the survival rate, decreased the climbing activity, elevated MDA concentration and AChE activities of flies. SOD, CAT and GST activities were also reduced in AlCl3treated flies. Vitamin E was able to improve the survival rate, restored AlCl3induced reduction in climbing activity, ameliorated AlCl3 increase in AChE activity and MDA concentration in flies. In addition, Vitamin E attenuated AlCl3induced inhibition of SOD, CAT and GST activities.ConclusionThis study has shown that Vitamin E has both antioxidant and anticholinesterase activities and can be regarded as a therapeutic agent against AlCl3 induced toxicity and associated diseases.

Vitamin E: Where Are We Now in Vascular Diseases?

Vitamin E is one of the most popular fat-soluble vitamins in pathological research and has been under scrutiny since the 1980s as a vital dietary component of food. The antioxidant effect of vitamin E has been widely studied due to its benefits in the prevention of various cardiovascular diseases. In recent years, alternative effects of vitamin E, in terms of anti-inflammatory pathways and gene regulation, have also been of interest to researchers. This review examines the role of dietary vitamin E (α-tocopherol) as an antioxidant and bioactive molecule in promoting vascular health. While the antioxidant effect of vitamin E is well established, knowledge about its capacity as a promising regulatory molecule in the control of the vascular system is limited. The aim of this review is to discuss some of these mechanisms and summarize their role in the prevention of cardiovascular diseases (CVD). Here, we also briefly discuss foods rich in vitamin E, and deliberate some potential toxicological effects of excessive supplemental vitamin E in the body.

A consideration on the effect of antioxidant vitamins on blood homocysteine levels

A consideration on the effect of antioxidant vitamins on blood homocysteine levels

Antioxidant effect of vitamin E on diphenylamine-induced hepato-renal oxidative stress and structural changes in rat fetuses

To date, studies on the effects of prenatal exposure to diphenylamine on developing fetuses are sparse. Therefore, further investigation is required to determine the potential prenatal hazard of this compound and to introduce possible treatment for these hazards. This study aimed to assess the biochemical, histopathological, and ultrastructural changes induced by diphenylamine in the developing liver and kidney of rat fetuses and the role of vitamin E in alleviating these changes. Fifty pregnant rats were divided equally into five groups, the group I was administrated distilled water, group II was administrated corn oil, group III was administrated 100 mg/kg/b.wt. vitamin E, group IV was administrated approximately 400 mg/kg/b.wt diphenylamine and group V was administrated diphenylamine + vitamin E at the above-mentioned doses from the 6th to 15th day of pregnancy. Diphenylamine induced undesirable histopathological and ultrastructural changes in the fetal liver and kidney. These changes were in the form of vacuolation, congestions of central veins, hemorrhage, leucocytic infiltration, degenerated cytoplasm, pyknotic nuclei, and swollen mitochondria and rER of hepatocytes. While the degenerative changes in the kidney were represented by degenerated brush border, lumen dilation, tubular hyalinization, vacuolation, degenerated nuclei, and mitochondria. Also, there was a significant decrease in the antioxidant enzymes i.e., superoxide dismutase and catalase, and a significant increase in reactive oxygen radicals and malondialdehyde. Treatment with vitamins E after diphenylamine restored all biochemical, histopathological, and ultrastructural damage cited above. In conclusion, vitamin E has antioxidant effects which could be able to antagonize diphenylamine prenatal toxicity.

Epigenetic regulation of oxidative and inflammatory phenotypes in women with gestational diabetes and offspring

Abstract Background Hyperglycemia-induced oxidative stress and inflammation are potent drivers of atherosclerotic cardiovascular disease (ASCVD). Gestational diabetes (GDM) is characterized by chronic hyperglycemia during pregnancy and may represent a clinical model to study the mechanisms of oxidative stress and inflammation induced by hyperglycemia. GDM is associated with a range of adverse perinatal and long-term outcomes for both mother and offspring. In this perspective, it is emerging a putative association between maternal GDM and offspring's epigenetic trait. Purpose To investigate the link between histone modifications, oxidative stress and inflammatory phenotype as well as the transmission of epigenetic signatures to the offspring. Methods We analyzed peripheral blood mononuclear cells (PBMC) from GDM and control mothers as well as human umbilical vein endothelial cells (HUVEC) and cord blood mononuclear cells (CBMC) isolated from newborn umbilical cords obtained at delivery from both groups. Histone methyltransferase MLL1-dependent trimethylation of histone 3 at lysine 4 amino residue (H3K4me3) on NF-kB p65 subunit promoter region was assessed by chromatin immunoprecipitation (ChIP) and real-time qPCR in HUVEC, PBMC and CBMC, respectively. MLL1 and downstream inflammatory and redox genes were determined by real-time qPCR and immunocytochemistry in the presence and in the absence of MLL1 inhibitor MM-102. Measurement of reactive oxygen species (ROS) was performed by electron spin resonance spectroscopy. Results For the first time, we demonstrated a significant increase of MLL1 expression with subsequent MLL1-induced upregulation of NF-kB p65 gene via H3K4me3 in GDM as compared to control cells. MLL1-driven epigenetic remodeling of NF-kB p65 promoter is upstream to the activation of inflammatory pathway. Indeed, treatment with MM-102 decreased H3K4me3 and blunted expression of NF-kB p65 as well as VCAM-1, MCP-1 and IL-6 genes. We also found that expression of ROS scavenger aldehyde dehydrogenase 2 is reduced, whereas pro-oxidant nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit NOX4 is upregulated. Interestingly, the increased ROS generation observed in GDM is involved in the upregulation of MLL1 as shown by the restoring effect of antioxidant vitamin C on MLL1 expression levels. Conclusions Our results suggest that a complex interplay between oxidative stress and histone modifications are responsible for the GDM maternal inflammatory and oxidative phenotypes and its transmission to the offspring. The deciphering of epigenetic-induced chromatin remodelling opens the perspective for pharmacological reprogramming of adverse chromatin changes to reduce the burden of early development of metabolic phenotypes and ASCVD. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): University G. d'Annunzio MIUR fundings Schematic figure

Lipid oxidation that is, and is not, inhibited by vitamin E: Consideration about physiological functions of vitamin E

Lipids are oxidized in vivo by multiple oxidizing species with different properties, some by regulated manner to produce physiological mediators, while others by random mechanisms to give detrimental products. Vitamin E plays an important role as a physiologically essential antioxidant to inhibit unregulated lipid peroxidation by scavenging lipid peroxyl radicals to break chain propagation independent of the type of free radicals which induce chain initiation. Kinetic data suggest that vitamin E does not act as an efficient scavenger of nitrogen dioxide radical, carbonate anion radical, and hypochlorite. The analysis of regio- and stereo-isomer distribution of the lipid oxidation products shows that, apart from lipid oxidation by CYP enzymes, the free radical-mediated lipid peroxidation is the major pathway of lipid oxidation taking place in humans. Compared with healthy subjects, the levels of racemic and trans,trans-hydro (pero)xyoctadecadienoates, specific biomarker of free radical lipid oxidation, are elevated in the plasma of patients including atherosclerosis and non-alcoholic fatty liver diseases. α-Tocopherol acts as a major antioxidant, while γ-tocopherol scavenges nitrogen dioxide radical, which induces lipid peroxidation, nitration of aromatic compounds and unsaturated fatty acids, and isomerization of cis-fatty acids to trans-fatty acids. It is essential to appreciate that the antioxidant effects of vitamin E depend on the nature of both oxidants and substrates being oxidized. Vitamin E, together with other antioxidants such as vitamin C, contributes to the inhibition of detrimental oxidation of biological molecules and thereby to the maintenance of human health and prevention of diseases.

Evaluating effects of electromagnetic fields on the total number and percentage of white blood cells in mice

To evaluate the effects of electromagnetic waves on the total number and percentage of white blood cells and also antioxidant effects of vitamin C on the effects radiation, 24 male mice (Balb/c) were used: control under the influence of low frequency electromagnetic waves and under the influence of waves with vitamin C. Total number of white blood cells in under the influence waves group significantly increased compared to control group, and also under the influence waves group with vitamin C because its antioxidant property is able to prevent the increasing impact of electromagnetic waves. The percentage of white blood cells in the under influence waves group did not significantly change compared to the control group and also, the under influence waves group with vitamin C had no significant change compared to the other group. The percentage of neutrophils in samples of the under influence waves group had significant decrease compared to control group but in the under influence waves group with vitamin C compared to the other group, this vitamin C could prevent a significant reduction in percentage of neutrophils. Our findings indicated that low electromagnetic fields have caused significant changes in the total number of white blood cells and percentage of neutrophils in mice. In the group that received vitamin C injection, significant changes were observed in the total number of white blood cells and percentage of neutrophils relative to the group under the influence of low electromagnetic waves, which indicates that vitamin C could restore the mean total number of white blood cells and percentage of neutrophils to normal value.

Effects of Antioxidant Vitamins, Curry Consumption, and Heavy Metal Levels on Metabolic Syndrome with Comorbidities: A Korean Community-Based Cross-Sectional Study.

The burden of metabolic syndrome (MetS) has increased worldwide, especially during the COVID-19 pandemic, and this phenomenon is related to environmental, dietary, and lifestyle risk factors. We aimed to determine the association between the levels of serum heavy metals, hs-CRP, vitamins, and curry intake and to predict risks of MetS based on marginal effects. A data set of 60,256 Koreans aged ≥ 15 years between 2009 and 2017 was used to obtain information on sociodemographic, lifestyle, family history characteristics, MetS, food intake survey, and serum heavy metals. Daily intake of vitamins was measured by a one-day 24 h recall, and curry consumption was calculated using a food frequency questionnaire. Serum heavy metal levels were quantified by graphite furnace atomic absorption spectrometry and using a mercury analyzer. We found that vitamin B1, B2, B3, C, and A intakes were significantly lower in subjects with than without MetS. In contrast, serum levels of Pb, Hg, Cd, vitamin A, E, and hs-CRP were significantly higher in subjects with MetS. The risk of MetS was significantly lower for high curry consumers than low curry consumers (adjusted odds ratio 0.85, 95%CI 0.74–0.98). The risks of MetS were reduced by 12% and 1%, when vitamin B1 and C intakes increased by one mg, respectively, but were increased by 14%, 3%, and 9%, when serum levels of Pb, Hg, and hs-CRP increased by one unit. These results show that the potential health benefits resulting from vitamin and curry intakes could protect the public against the dual burden of communicable and non-communicable diseases. Further studies are required to reduce risk factors associated with serum heavy metal levels and to determine whether interactions between vitamin and curry consumption influence the presence of MetS.

Does vitamin C minimise exercise-induced oxidative stress?

Oxidative stress occurs when there is an imbalance between the production of free radicals and the detoxification of these reactive products. Regular exercise greatly increases the production of free radicals in humans, while excessive exercise could lead to cellular and tissue damage. This paper presents a review of studies focusing on exercise-induced oxidative stress, sufficient intensity of aerobic or anaerobic exercises, and how exercise volume and duration could increase free radicals in humans. Furthermore, this review examines the effects of chronic or acute vitamin C supplementation in minimising oxidative stress during exercise. In this regard, vitamin C is commonly consumed as an antioxidant supplement by endurance athletes to minimise exercise-induced oxidative stress, augment recovery and improve performance. However, there is still a lack of evidence regarding the antioxidant effects of vitamin C supplements during exercise. Based on the review, it could be concluded healthy, physically active individuals might not require regular intakes of non-physiological dosages of vitamin C. On the other hand, studies found that regular exercise could lead to higher antioxidant production that could be beneficial in mitigating oxidative stress and improving individuals’ health.

The Potential Anti-Obesity, Anti-Diabetic and Anti-Oxidant Effects of Vitamin a in Streptozotocin-Induced Diabetic Mice

Background: Evidence suggests that there is a link between diabetes mellitus and Vitamin A. Moreover, it has been reported that diabetes induces oxidative stress. Lately, a wide attention has been developed to the protective biochemical function of natural antioxidants contained vitamins, which can reduce the oxidative damage caused by free radical species.&#x0D; Objective: To investigate the anti-obesity, anti-diabetic and anti-oxidative effects of vitamin A in streptozotocin (STZ)-induced diabetic mice.&#x0D; Methods: Male mice were randomly divided into three groups: Control- nondiabetic, received a normal diet and water; Control-diabetic, received STZ 45mg/kg once intraperitoneally; and Treated-diabetic, received both STZ as before plus Vitamin A (4-IU/day) orally daily for 16 weeks. Food intake, body weight, fat mass, fasting blood glucose, serum insulin, and lipid profile were estimated. Also, superoxide dismutase (SOD), glutathione peroxidase (GPO), catalase (CAT), and malonaldehyde (MDA) were measured.&#x0D; Results: Treated diabetic mice with Vitamin A showed a significant improvement in their body weight, fat mass, lipid profile as well as SOD, GPO and CAT compared to Control-diabetic mice. However, Vitamin A caused no significant change on fasting blood glucose and insulin levels. Furthermore, plasma level of MDA was significantly elevated in diabetic mice compared to normal mice. Diabetic mice treated with vitamin A had a significantly reduced level of MDA, suggesting that vitamin A might have a vital role in the protection of tissues from damage by free radicals.&#x0D; Conclusion: Supplementation with vitamin A may be a useful treatment strategy for diabetic patients to reduce/prevent the pathological complications of diabetes.

Implant survival of 2,723 vitamin E-infused highly crosslinked polyethylene liners in total hip arthroplasty: data from the Finnish Arthroplasty Register

Background and purpose — The use of crosslinked polyethylene in total hip arthroplasty (THA) has decreased wear remarkably. It has been suggested that the antioxidative effects of vitamin E may enhance the wear properties of polyethylene even further. This study evaluates revision rates between vitamin E-infused polyethylene liners (E1 and E-poly, ZimmerBiomet, Warsaw, IN, USA) versus moderately crosslinked polyethylene (ModXLPE) liners from the same manufacturer used in primary THA. Patients and methods — We conducted a study based on data from the Finnish Arthroplasty Register. The study group consisted of 2,723 THAs with a vitamin E-infused liner and a reference group of 2,707 THAs with a moderately crosslinked polyethylene liner. Survivorship, revision risk, and re-revision causes were compared between groups. Results — The 7-year survival of the vitamin E-infused polyethylene liner group and of the reference group with revision for any reason as the endpoint was comparable (94% [95% CI 92.9–94.9] and 93% [CI 91.9–93.9], respectively). The adjusted hazard ratio (HR) for any revision was similar between the groups (0.7 [CI 0.4–1.1]). When revision for aseptic loosening was studied as the endpoint, the survival for the study group was 99% (CI 98.6–99.4) and for the reference group 99% (CI 98.7–99.5), and the risk of revision was comparable between the study groups (HR 1.3 [CI 0.7–2.5]). Interpretation — After an observation period of 7 years vitamin E-infused liners shows results equal to results obtained with crosslinked polyethylene liners.

Antioxidant effect of Vitamin E on the male rat reproductive system by a high oral dose of Bisphenol-A

Among researchers, environmental pollutants and their contribution to male fertility are still being discussed. The use of antioxidants manages to boost the reproductive system with the scavenging of free radicals. This study aimed to investigate the inhibiting function of Vitamin E (VE) on Bisphenol-A (BPA) toxicity in the male rats’ reproductive system. Male rats were divided into 4 groups: control (negative control) group, BPA group treated by 250 mg/kg/day (positive control), VE group treated by 150 mg/kg/day (comparative control) and BPA + VE group that received both doses at the same time (Oral treatment by gavage; 56 days). Sperm parameters, testicular tissue morphometric and biochemical tests were evaluated. Sperm count, motility, viability, normal morphology, sperm tail length, spermatogenesis index and serum testosterone levels significantly decreased in the BPA group compared to the control group. Versus a significant enhancement in the positive-TUNEL germinal cells and serum malondialdehyde (MDA) levels were observed. Moreover, BPA exhibited no effect on sperm maturity and DNA integrity. In the simultaneous treatment group (BPA + EV), VE could improve and regulate all the mentioned parameters within the control group range. As mentioned, there was a significant difference in the results in the positive control group compared to the negative control group. But these data improved significantly in the BPA + VE. It can be concluded that in this group, VE was able to overcome the toxicity caused by positive control in their simultaneous treatment and maintain the data at the negative control group range. Therefore, no significant change was observed in the BPA + VE group compared to the negative control group.

Antioxidant Effect of Vitamin in Exercise and the Effect of Physical Supplement

Antioxidant Effect of Vitamin in Exercise and the Effect of Physical Supplement

Kronik Böbrek Yetmezliğinde Antioksidan Vitaminlerin İnflamasyon ve Oksidatif Stres Üzerine Etkisi

Kronik böbrek yetmezliği (KBY), inflamasyonun ve oksidatif stresin sıklıkla eşlik ettiği bir süreç olarak bilinmektedir. Kronik böbrek yetmezliği hastalarında artan oksidatif stres düzeyleri, azalmış antioksidan savunma ve ortaya çıkan kronik inflamasyon kardiyovasküler hastalıklar başta olmak üzere birçok sağlık sorunu için risk faktörü olabilmektedir. Bu nedenle hastalarda antioksidan tedavinin uygun kullanımı oldukça önem taşımaktadır. Antioksidan vitaminlerin sürece etkisi değerlendirildiğinde, KBY hastalarında retinol bağlayıcı protein katabolizmasındaki azalmalar nedeniyle serum A vitamini konsantrasyonlarının sıklıkla yüksek olduğu düşünülmektedir. Buna bağlı olarak KBY hastalarına ek A vitamini suplemantasyonu önerilmemektedir. Diğer bir antioksidan olan C vitamininin, prooksidan etki gösterebilme ve oksalat oluşumunu artırma riski nedeniyle bu hastalara yönelik öneri konusu tartışmalıdır. Ancak diyaliz tedavisi alan hastalar değerlendirilirken C vitamininde gözlenen önemli kayıplar ve diyet kısıtlılıkları nedeniyle alımdaki azalmalar dikkate alınmalıdır. Kronik böbrek yetmezliği hastalarında E vitamininin birçok olumlu etkisi bildirilmekle birlikte suplemantasyonun dozu, süresi ve uygulama yolu gibi farklılıklar nedeniyle net öneri vermek mümkün olmamaktadır. Bununla birlikte özellikle E vitamini kaplı diyaliz membran kullanımının oksidatif stresi azaltabileceği düşünülmektedir. Kronik böbrek yetmezliği hastalarında antioksidan vitamin desteğine yönelik çalışmaların devam etmesi gerekmekle birlikte, hastaların diyet antioksidan vitamin alımlarının iyi değerlendirilmesi oldukça önem taşımaktadır.

Effects of vitamin E in a glucocorticoid induced cataract model in chicken embryos

ABSTRACT We investigated the antioxidant effects of vitamin E on a glucocorticoid (GC) induced model of cataracts in chick embryos. We used 70 fertilized eggs divided into seven groups as follows: phosphate-buffered saline (PBS) group, olive oil treatment (OO) group, hydrocortisone treatment (HC) group, olive oil and hydrocortisone treatment (OO + HC) group, 50 mg/kg vitamin E and hydrocortisone treatment (HC + VE (50)) group, 25 mg/kg vitamin E and hydrocortisone treatment (HC + VE (25)) group and 15 mg/kg vitamin E and hydrocortisone treatment (HC + VE (15)) group. On day 17, chick embryos were removed from the eggs and lens and liver tissues were excised. Cataract formation was evaluated and total antioxidant status (TAS), total oxidant status (TOS), malondialdehyde (MDA) and glutathione peroxidase (GPx) were measured in lens and liver tissues; MDA was measured only in liver. The lenses in the HC + VE (50) group exhibited significantly higher levels of GPx and TAS, and lower levels of TOS than for HC and OO + HC groups. The livers of the HC + VE (50) group exhibited significantly higher levels of GPx and lower levels of MDA than for the HC and OO + HC groups. The HC + VE (50) group lenses were evaluated as grade 1, because the nuclei were completely free of cataracts, likely due to the antioxidative effect of high dose VE. VE is an effective antioxidant agent that exhibits a dose-response effect, for ameliorating the negative effects of GCs.