Manuka honey protects middle-aged rats from oxidative damage

OBJECTIVE: This study aimed to determine the effect of manuka honey on the oxidative status of middle-aged rats. METHOD: Twenty-four male Sprague-Dawley rats were divided into young (2 months) and middle-aged (9 months) groups. They were further divided into two groups each, which were either fed with plain water (control) or supplemented with 2.5 g/kg body weight of manuka honey for 30 days. The DNA damage level was determined via the comet assay, the plasma malondialdehyde level was determined using high performance liquid chromatography, and the antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase, glutathione peroxidase and catalase) were determined spectrophotometrically in the erythrocytes and liver. The antioxidant activities were measured using 1,1-diphenyl-2-picrylhydrazyl and ferric reducing/antioxidant power assays, and the total phenolic content of the manuka was analyzed using UV spectrophotometry and the Folin-Ciocalteu method, respectively. RESULTS: Supplementation with manuka honey reduced the level of DNA damage, the malondialdehyde level and the glutathione peroxidase activity in the liver of both the young and middle-aged groups. However, the glutathione peroxidase activity was increased in the erythrocytes of middle-aged rats given manuka honey supplementation. The catalase activity was reduced in the liver and erythrocytes of both young and middle-aged rats given supplementation. Manuka honey was found to have antioxidant activity and to have a high total phenolic content. These findings showed a strong correlation between the total phenolic content and antioxidant activity. CONCLUSIONS: Manuka honey reduces oxidative damage in young and middle-aged rats; this effect could be mediated through the modulation of its antioxidant enzyme activities and its high total phenolic content. Manuka honey can be used as an alternative supplement at an early age to improve the oxidative status

Uncoupling healthspan and lifespan in long lived Daf-2, Pmk-3 and Sgk-1 knockdown Caenorhabditis elegans

Modulation of genes expression in signaling pathways promotes longevity in Caenorhabditis elegans (C. elegans) but it is unclear whether this will improve healthspan. This study aimed to determine the healthspan of daf-2, pmk-3 and sgk-1 knocked-down worms. Health measures were determined at day 5, day 10 and day 15 of adult worms which were cultured in nematode growth media containing Escherichia coli. Heat resistance was determined by analysing the survival of worms at 37°C. Oxidative stress resistance was measured after exposure to 10mM hydrogen peroxide to analyse its survival capacity. Movement capacity was analysed by computing the distance travelled on solid media and the number of thrashing in liquid media. Results showed that the gene knockdown worms survived longer than wildtype worms. Daf-2 and pmk-3 knockdown increased movement capacity at day 5 and 10 in solid and liquid media but resulted in similar capacities to wildtype worms at day 15. Sgk-1 knockdown increased movement capacity only at day 5 in both media. The ability of gene knocked-down worms to withstand heat and oxidative stress significantly increased. In conclusion, knockdown of daf-2, pmk-3 and sgk-1 improved resistance to heat and oxidative stress but did not modulate movement incompetency at advanced ages C. elegans

Effect of the tocotrienol-rich fraction on the lifespan and oxidative biomarkers in Caenorhabditis elegans under oxidative stress

OBJECTIVE: This study was performed to determine the effect of the tocotrienol-rich fraction on the lifespan and oxidative status of C. elegans under oxidative stress. METHOD: Lifespan was determined by counting the number of surviving nematodes daily under a dissecting microscope after treatment with hydrogen peroxide and the tocotrienol-rich fraction. The evaluated oxidative markers included lipofuscin, which was measured using a fluorescent microscope, and protein carbonyl and 8-hydroxy-2′-deoxyguanosine, which were measured using commercially available kits. RESULTS: Hydrogen peroxide-induced oxidative stress significantly decreased the mean lifespan of C. elegans, which was restored to that of the control by the tocotrienol-rich fraction when administered before or both before and after the hydrogen peroxide. The accumulation of the age marker lipofuscin, which increased with hydrogen peroxide exposure, was decreased with upon treatment with the tocotrienol-rich fraction (

Comparing the effects of vitamin E tocotrienol-rich fraction supplementation and α-tocopherol supplementation on gene expression in healthy older adults

OBJECTIVES: This study aims to compare the differential gene expression resulting from tocotrienol-rich fraction and α-tocopherol supplementation in healthy older adults. METHODS: A total of 71 eligible subjects aged 50 to 55 years from Gombak and Kuala Lumpur, Malaysia, were divided into three groups and supplemented with placebo (n=23), α-tocopherol (n=24) or tocotrienol-rich fraction (n=24). Blood samples were collected at baseline and at 3 and 6 months of supplementation for microarray analysis. RESULTS: The number of genes altered by α-tocopherol was higher after 6 months (1,410) than after 3 months (273) of supplementation. α-Tocopherol altered the expression of more genes in males (952) than in females (731). Similarly, tocotrienol-rich fraction modulated the expression of more genes after 6 months (1,084) than after 3 months (596) and affected more genes in males (899) than in females (781). α-Tocopherol supplementation modulated pathways involving the response to stress and stimuli, the immune response, the response to hypoxia and bacteria, the metabolism of toxins and xenobiotics, mitosis, and synaptic transmission as well as activated the mitogen-activated protein kinase and complement pathways after 6 months. However, tocotrienol-rich fraction supplementation affected pathways such as the signal transduction, apoptosis, nuclear factor kappa B kinase, cascade extracellular signal-regulated kinase-1 and extracellular signal-regulated kinase-2, immune response, response to drug, cell adhesion, multicellular organismal development and G protein signaling pathways. CONCLUSION: Supplementation with either α-tocopherol or tocotrienol-rich fraction affected the immune and drug response and the cell adhesion and signal transduction pathways but modulated other pathways differently after 6 months of supplementation, with sex-specific responses

Effects of Microalgae on Metabolic Syndrome

Metabolic syndrome (MetS) is a cluster of metabolic disturbances, including abdominal obesity, hypertension, hypertriglyceridemia, reduced high-density lipoprotein cholesterol (HDL-C) and hyperglycemia. Adopting a healthier lifestyle and multiple drug-based therapies are current ways to manage MetS, but they have limited efficacy, albeit the prevalence of MetS is rising. Microalgae is a part of the human diet and has also been consumed as a health supplement to improve insulin sensitivity, inflammation, and several components of MetS. These therapeutic effects of microalgae are attributed to the bioactive compounds present in them that exhibit antioxidant, anti-inflammatory, anti-obesity, antihypertensive, hepatoprotective and immunomodulatory effects. Therefore, studies investigating the potential of microalgae in alleviating MetS are becoming more popular, but a review on this topic remains scarce. In this review, we discuss the effects of microalgae, specifically on MetS, by reviewing the evidence from scientific literature covering in vitro and in vivo studies. In addition, we also discuss the underlying mechanisms that modulate the effects of microalgae on MetS, and the limitations and future perspectives of developing microalgae as a health supplement for MetS. Microalgae supplementation is becoming a viable approach in alleviating metabolic disturbances and as a unique addition to the management of MetS

Differential protein expression in senescent human skin fibroblasts and stress induced premature senescence (SIPS) fibroblasts

Replicative senescence of human diploid fibroblasts (HDFs) occurs when cells lose their capacity to proliferate and enter a phase of irreversible growth arrest. Stress-induced premature senescence (SIPS) on the other hand is caused by subcytotoxic concentrations of various oxidants which trigger accelerated cellular senescence. In this study, a SIPS model was established by exposing human diploid fibroblasts (HDFs) to 20 μM H2O2 for 2 weeks. A proteomic comparison between young, senescent and SIPS cells was done using two dimensional gel electrophoresis (2DGE) to elucidate the changes in protein expression associated with cellular aging. Our analysis showed that 28 protein spots were differentially expressed in senescent cells whereas 10 protein spots were differentially expressed in SIPS as compared to young cells. Three similar protein spots were differentially expressed in both senescent and SIPS cells when compared to the young cells. These results indicate that a difference in protein expression exists between senescent cells and SIPS cells compared to young cells

Effect of the tocotrienol-rich fraction on the lifespan and oxidative biomarkers in Caenorhabditis elegans under oxidative stress

OBJECTIVE: This study was performed to determine the effect of the tocotrienol-rich fraction on the lifespan and oxidative status of C. elegans under oxidative stress. METHOD: Lifespan was determined by counting the number of surviving nematodes daily under a dissecting microscope after treatment with hydrogen peroxide and the tocotrienol-rich fraction. The evaluated oxidative markers included lipofuscin, which was measured using a fluorescent microscope, and protein carbonyl and 8-hydroxy-2&#8242;-deoxyguanosine, which were measured using commercially available kits. RESULTS: Hydrogen peroxide-induced oxidative stress significantly decreased the mean lifespan of C. elegans, which was restored to that of the control by the tocotrienol-rich fraction when administered before or both before and after the hydrogen peroxide. The accumulation of the age marker lipofuscin, which increased with hydrogen peroxide exposure, was decreased with upon treatment with the tocotrienol-rich fraction (p<0.05). The level of 8-hydroxy-2&#8242;-deoxyguanosine significantly increased in the hydrogen peroxide-induced group relative to the control. Treatment with the tocotrienol-rich fraction before or after hydrogen peroxide induction also increased the level of 8-hydroxy-2&#8242;-deoxyguanosine relative to the control. However, neither hydrogen peroxide nor the tocotrienol-rich fraction treatment affected the protein carbonyl content of the nematodes. CONCLUSION: The tocotrienol-rich fraction restored the lifespan of oxidative stress-induced C. elegans and reduced the accumulation of lipofuscin but did not affect protein damage. In addition, DNA oxidation was increased

Comparing Palm Oil, Tocotrienol-Rich Fraction and α-Tocopherol Supplementation on the Antioxidant Levels of Older Adults

Background: Tocotrienol and tocopherol are known to prevent numerous degenerative diseases. The aim of this study is to compare the effects of tocotrienol-rich fraction (TRF) with α-tocopherol (α-TF) on the antioxidant status of healthy individuals aged between 50 and 55 years. Methods: Volunteers were divided into groups receiving placebo (n = 23), α-TF (n = 24) and TRF (n = 24). Fasting venous blood samples were taken at baseline (0 month), 3 months and 6 months of supplementation for the determination of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities as well as for reduced glutathione (GSH) and oxidized glutathione (GSSG) concentrations. Results: CAT and GPx were unaffected by TRF and α-TF supplementations. SOD activity increased significantly after six months of TRF supplementation. Analysis by gender showed that only female subjects had significant increases in SOD and GPx activities after six months of TRF supplementation. GPx activity was also significantly higher in females compared to males after six months of TRF supplementation. The GSH/GSSG ratio increased significantly after six months of TRF and α-TF supplementation in only the female subjects. Conclusion: TRF and α-TF supplementation exhibited similar effects to the antioxidant levels of older adults with TRF having more significant effects in females

A Review of the Effects of Fucoxanthin on NAFLD

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of chronic liver disease. Fucoxanthin, a red-orange marine carotenoid, is found in natural marine seaweeds with high antioxidant activity and several other remarkable biological features. The aim of this review is to gather evidence of the positive benefits of fucoxanthin on NAFLD. Fucoxanthin provides an extensive list of physiological and biological properties, such as hepatoprotective, anti-obesity, anti-tumor, and anti-diabetes properties, in addition to antioxidant and anti-inflammatory properties. This review focuses on published research on the preventative effects of fucoxanthin on NAFLD from the perspective of human clinical trials, animal experiments in vivo, and in vitro cell investigations. Using a variety of experimental designs, including treatment dosage, experiment model, and experimental periods, the positive effects of fucoxanthin were demonstrated. Fucoxanthin’s biological activities were outlined, with an emphasis on its therapeutic efficacy in NAFLD. Fucoxanthin showed beneficial effects in modulating lipid metabolism, lipogenesis, fatty acid oxidation, adipogenesis, and oxidative stress on NAFLD. A deeper comprehension of NAFLD pathogenesis is essential for the development of novel and effective therapeutic strategies