Catechin induced longevity in C. elegans: From key regulator genes to disposable soma

Saul, Nadine; Pietsch, Kerstin; Menzel, Ralph; Stürzenbaum, Stephen R.; Steinberg, Christian E. W.

doi:10.1016/j.mad.2009.05.005

Cited by 120 publications

(126 citation statements)

References 116 publications

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“…PPs are a potent substance class of phytochemicals, and some are capable to significantly extend the lifespan of the nematode C. elegans (summarized in Saul et al 2009). They are able to induce a vast array of phenotypic responses, thus further in-depth investigations are called for to rule out artifacts associated with respective test-designs and decipher the exact underlying mechanisms that drive the observed effects.…”

Section: Discussionmentioning

confidence: 99%

“…To unravel the underlying genetics of CA and RA action in vivo, we carried out lifespan assays with selected C. elegans mutant strains lacking genes previously implicated in stress response or aging Saul et al 2009Saul et al , 2010. It is intriguing that CA and RA was not able to significantly extend lifespan in four mutant strains (osr-1, sek-1, sir-2.1 and unc-43) ( Fig.…”

Section: Is Longevity Offset By Other Physiological Trade-offs?mentioning

confidence: 99%

“…This has been elegantly demonstrated in mice and Drosophila melanogaster, where a reduction in body size correlates with longevity (Flurkey et al 2001;Nielsen et al 2008) but also in C. elegans, where Harrington and Harley (1988) observed a reduction of offspring in response to Vitamin E mediated longevity. Similarly, Saul et al (2009Saul et al ( , 2010 discovered that Catechin and Tannic acid mediated longevity was associated with an attenuation of growth. These findings encouraged us to study several fitness parameters to verify whether physiological trade-offs occur in C. elegans.…”

Section: Fitness Alterations and Trade-offs Of Vital Parameters?mentioning

confidence: 99%

“…In addition to the basic provision of energy and essential micronutrients, plant-based foods also contain thousands of biologically active and interacting phytochemicals that are thought to be instrumental in preventing disease and promoting health (Liu 2004). Indeed, studies with the model organism C. elegans show promise in the efficacy of certain polyphenols (PPs) in reversing the age-related decline and thereby driving longevity (Resveratrol, Wood et al 2004;Blueberry Polyphenols, Wilson et al 2006;Quercetin, Catechin, Tannic acid, Saul et al 2008Quercetin, Caffeic acid, Pietsch et al 2009; and many others, summarized in Saul et al 2009).…”

Section: Introductionmentioning

confidence: 99%

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Hormetins, antioxidants and prooxidants: defining quercetin-, caffeic acid- and rosmarinic acid-mediated life extension in C. elegans

et al. 2011

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Quercetin, Caffeic- and Rosmarinic acid exposure extend lifespan in Caenorhabditis elegans. This comparative study uncovers basic common and contrasting underlying mechanisms: For all three compounds, life extension was characterized by hormetic dose response curves, but hsp-level expression was variable. Quercetin and Rosmarinic acid both suppressed bacterial growth; however, antibacterial properties were not the dominant reason for life extension. Exposure to Quercetin, Caffeic- and Rosmarinic acid resulted in reduced body size, altered lipid-metabolism and a tendency towards a delay in reproductive timing; however the total number of offspring was not affected. An indirect dietary restriction effect, provoked by either chemo-repulsion or diminished pharyngeal pumping was rejected. Quercetin and Caffeic acid were shown to increase the antioxidative capacity in vivo and, by means of a lipofuscin assay, reduce the oxidative damage in the nematodes. Finally, it was possible to demonstrate that the life and thermotolerance enhancing properties of Caffeic- and Rosmarinic acid both rely on osr-1, sek-1, sir-2.1 and unc-43 plus daf-16 in the case of Caffeic acid. Taken together, hormesis, in vivo antioxidative/prooxidative properties, modulation of genetic players, as well as the re-allocation of energy all contribute (to some extent and dependent on the polyphenol) to life extension.

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Section: Discussionmentioning

confidence: 99%

Section: Is Longevity Offset By Other Physiological Trade-offs?mentioning

confidence: 99%

Section: Fitness Alterations and Trade-offs Of Vital Parameters?mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hormetins, antioxidants and prooxidants: defining quercetin-, caffeic acid- and rosmarinic acid-mediated life extension in C. elegans

et al. 2011

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“…Poor food quality corresponds mainly to caloric restriction in evaluation aging mechanisms, which is well known as a non-genetic intervention that robustly extends lifespan in a variety of species (Masoro, 2005;Kaeberlein et al, 2006;Lee et al, 2006;Castelein et al, 2008;Pietsch et al, 2009;Saul et al, 2009). It is commonly thought that a reduction of reactive oxygen species, ROS, plays a pivotal role.…”

Section: Humic Substances As Stressormentioning

confidence: 99%

Stress by poor food quality and exposure to humic substances: Daphnia magna responds with oxidative stress, lifespan extension, but reduced offspring numbers

et al. 2010

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In freshwater systems, many abiotic and biotic factors determine the natural fluctuation of Daphnia spec. populations: climatic and water quality parameters, quantitative and qualitative food quality and quantity, predation, and humic substances. Many factors/stressors act in concert. In this contribution, we supplied Daphnia magna with two different diets (chlorococcal alga Pseudokirchneriella subcapitata and baker's yeast) fed ad libitum and exposed it to an environmentally realistic concentration of humic substances (HSs). Exposure to HSs caused a transcriptionally controlled stress response with studied genes; cat and hsp60, for the latter partial sequences have been identified. Furthermore, the exposure to HSs reduced the antioxidant capacity. Yet, a much stronger oxidative stress is caused by feeding yeast, which reduced the anti-oxidative capacity to values of approximately 50% of the green algal diet. This reduction is most likely due to the yeast's cell wall to resist digestion rather than to the elemental ratio or deficiency in long-chained unsaturated fatty acids, because both diets were deficient in fatty acids with back bones of more than 20 C-atoms. We assume that the biochemical machinery in the gut continuously activated oxygen to cleave the yeast's cell wall and, hence, reduced the antioxidative capacity of the animals. Neither the analyzed oxidant, H 2 O 2 , nor the antioxidants, total apparent ascorbic acid nor free proline, reflected the oxidative stress situations properly. In addition to the stress, HS exposure extended the mean lifespan of algae-fed D. magna, but at the expense of offspring numbers; so did also the pure yeast diet as compared to the algae diet. The first lifespan extension can be explained by the potential of HSs to block the pathway via the insulin-like growth factor 1 (IGF), whereas the second matches the, in aging papers, well described, but Electronic supplementary material The online version of this article (mechanistically poorly understood caloric restriction. Yeast-fed animals, exposed to HSs changed the energy allocation by reducing life span, but increasing offspring numbers. With the lifespan and offspring numbers, ecologically relevant parameters are differently affected by the simultaneous action of two environmentally relevant stressors.

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Curcumin and neurodegenerative diseases

2013

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Over the last ten years curcumin has been reported to be effective against a wide variety of diseases and is characterized as having anti-carcinogenic, hepatoprotective, thrombosuppressive, cardioprotective, anti-arthritic, and anti-infectious properties. Recent studies performed in both vertebrate and invertebrate models have been conducted to determine whether curcumin was also neuroprotective. The efficacy of curcumin in several pre-clinical trials for neurodegenerative diseases has created considerable excitement mainly due to its lack of toxicity and low cost. This suggests that curcumin could be a worthy candidate for nutraceutical intervention. Since aging is a common risk factor for neurodegenerative diseases, it is possible that some compounds that target aging mechanisms could also prevent these kinds of diseases. One potential mechanism to explain several of the general health benefits associated with curcumin is that it may prevent aging-associated changes in cellular proteins that lead to protein insolubility and aggregation. This loss in protein homeostasis is associated with several age-related diseases. Recently, curcumin has been found to help maintain protein homeostasis and extend lifespan in the model invertebrate Caenorhabditis elegans. Here, we review the evidence from several animal models that curcumin improves healthspan by preventing or delaying the onset of various neurodegenerative diseases.

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Catechin induced longevity in C. elegans: From key regulator genes to disposable soma

Cited by 120 publications

References 116 publications

Hormetins, antioxidants and prooxidants: defining quercetin-, caffeic acid- and rosmarinic acid-mediated life extension in C. elegans

Hormetins, antioxidants and prooxidants: defining quercetin-, caffeic acid- and rosmarinic acid-mediated life extension in C. elegans

Stress by poor food quality and exposure to humic substances: Daphnia magna responds with oxidative stress, lifespan extension, but reduced offspring numbers

Curcumin and neurodegenerative diseases

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