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Curcumin-supplemented diets increase superoxide dismutase activity and mean lifespan in Drosophila.

ABSTRACT: Curcumin is a polyphenolic bioactive compound in turmeric. We examined if antioxidant effects of curcumin are associated with lifespan extension in Drosophila. In this experiment, females and males of Drosophila were fed diets either containing no curcumin (C0) or supplemented with curcumin at 0.5 (C1) and 1.0 (C2) mg/g of diet. The levels of malondialdehyde (MDA), enzyme activity of superoxide dismutase (SOD), and expression of seven age-related genes in females and males were analyzed. We found that C1 and C2 increased mean lifespan by 6.2 % and 25.8 % in females, and by 15.5 % and 12.6 % in males, respectively. Meanwhile, C1 and C2 significantly decreased MDA levels and increased SOD activity in both genders. Diets C1 in females and C2 in males are effective in extending mean lifespan and improving levels of two physiological and biochemical measures related to aging in Drosophila. Lifespan extension of curcumin in Drosophila was associated with the up-regulation of Mn-SOD and CuZn-SOD genes, and the down-regulation of dInR, ATTD, Def, CecB, and DptB genes. The present results suggest that curcumin increases mean lifespan of Drosophila via regulating gene expression of the key enzyme SOD and reducing accumulation of MDA and lipid peroxidation. This study provided new insights for understanding the anti-aging mechanism of curcumin in Drosophila.

SUBMITTER: Shen LR

PROVIDER: S-EPMC3705117 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature

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Curcumin-supplemented diets increase superoxide dismutase activity and mean lifespan in Drosophila.

Shen Li-Rong LR Xiao Fa F Yuan Peng P Chen Ying Y Gao Qi-Kang QK Parnell Laurence D LD Meydani Mohsen M Ordovas Jose M JM Li Duo D Lai Chao-Qiang CQ

Age (Dordrecht, Netherlands) 20120601 4

Curcumin is a polyphenolic bioactive compound in turmeric. We examined if antioxidant effects of curcumin are associated with lifespan extension in Drosophila. In this experiment, females and males of Drosophila were fed diets either containing no curcumin (C0) or supplemented with curcumin at 0.5 (C1) and 1.0 (C2) mg/g of diet. The levels of malondialdehyde (MDA), enzyme activity of superoxide dismutase (SOD), and expression of seven age-related genes in females and males were analyzed. We foun ...[more]

PMID: 22653297

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Project description:The oxidative stress theory of aging postulates that aging results from the accumulation of molecular damage caused by reactive oxygen species (ROS) generated during normal metabolism. Superoxide dismutases (SODs) counteract this process by detoxifying superoxide. It has previously been shown that elimination of either cytoplasmic or mitochondrial SOD in yeast, flies, and mice results in decreased lifespan. In this experiment, we examine the effect of eliminating each of the five individual sod genes present in Caenorhabditis elegans. In contrast to what is observed in other model organisms, none of the sod deletion mutants shows decreased lifespan compared to wild-type worms, despite a clear increase in sensitivity to paraquat- and juglone-induced oxidative stress. In fact, even mutants lacking combinations of two or three sod genes survive at least as long as wild-type worms. Examination of gene expression in these mutants reveals mild compensatory up-regulation of other sod genes. Interestingly, we find that sod-2 mutants are long-lived despite a significant increase in oxidatively damaged proteins. Testing the effect of sod-2 deletion on known pathways of lifespan extension reveals a clear interaction with genes that affect mitochondrial function: sod-2 deletion markedly increases lifespan in clk-1 worms while clearly decreasing the lifespan of isp-1 worms. Combined with the mitochondrial localization of SOD-2 and the fact that sod-2 mutant worms exhibit phenotypes that are characteristic of long-lived mitochondrial mutants-including slow development, low brood size, and slow defecation-this suggests that deletion of sod-2 extends lifespan through a similar mechanism. This conclusion is supported by our demonstration of decreased oxygen consumption in sod-2 mutant worms. Overall, we show that increased oxidative stress caused by deletion of sod genes does not result in decreased lifespan in C. elegans and that deletion of sod-2 extends worm lifespan by altering mitochondrial function.

Project description:ImportanceX-linked adrenoleukodystrophy (ALD) may switch phenotype to the fatal cerebral form (ie, cerebral ALD [cALD]), the cause of which is unknown. Determining differences in antioxidant capacity and superoxide dismutase (SOD) levels between phenotypes may allow for the generation of a clinical biomarker for predicting the onset of cALD, as well as initiating a more timely lifesaving therapy.ObjectiveTo identify variations in the levels of antioxidant capacity and SOD activity between ALD phenotypes in patients with cALD or adrenomyeloneuropathy (AMN), heterozygote female carriers, and healthy controls and, in addition, correlate antioxidant levels with clinical outcome scores to determine a possible predictive value.Design, setting, and participantsSamples of monocytes and blood plasma were prospectively collected from healthy controls, heterozygote female carriers, and patients with AMN or cALD. We are counting each patient as 1 sample in our study. Because adrenoleukodystrophy is an X-linked disease, the affected group populations of cALD and AMN are all male. The heterozygote carriers are all female. The samples were assayed for total antioxidant capacity and SOD activity. The data were collected in an academic hospital setting. Eligibility criteria included patients who received a diagnosis of ALD and heterozygote female carriers, both of which groups were compared with age-matched controls. The prospective samples (n = 30) were collected between January 2015 to January 2016, and existing samples were collected from tissue storage banks at the Kennedy Krieger Institute (n = 30). The analyses were performed during the first 3 months of 2016.Main outcome and measuresCommercially available total antioxidant capacity and SOD assays were performed on samples of monocytes and blood plasma and correlated with magnetic resonance imaging severity score.ResultsA reduction in antioxidant capacity was shown between the healthy controls (0.225 mmol trolox equivalent) and heterozygote carriers (0.181 mmol trolox equivalent), and significant reductions were seen between healthy controls and patients with AMN (0.102 mmol trolox equivalent; P < .01), as well as healthy controls and patients with cALD (0.042 mmol trolox equivalent; P < .01). Superoxide dismutase activity in human blood plasma mirrored these reductions between prospectively collected samples from healthy controls (2.66 units/mg protein) and samples from heterozygote female carriers (1.91 units/mg protein), patients with AMN (1.39 units/mg protein; P = .01), and patients with cALD (0.8 units/mg protein; P < .01). Further analysis of SOD activity in biobank samples showed significant reductions between patients with AMN (0.89 units/mg protein) and patients with cALD (0.18 units/mg protein) (P = .03). Plasma SOD levels from patients with cALD demonstrated an inverse correlation to brain magnetic resonance imaging severity score (R2 = 0.75, P < .002). Longitudinal plasma SOD samples from the same patients (n = 4) showed decreased activity prior to and at the time of cerebral diagnosis over a period of 13 to 42 months (mean period, 24 months).Conclusions and relevancePlasma SOD may serve as a potential biomarker for cerebral disease in ALD following future prospective studies.

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Curcumin-supplemented diets increase superoxide dismutase activity and mean lifespan in Drosophila.

Publications

Curcumin-supplemented diets increase superoxide dismutase activity and mean lifespan in Drosophila.

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