China
Africa
Explore chapters and articles related to this topic
Soybean-Based Functional Foods Through Microbial Fermentation: Processing and Biological Activities
Published in Megh R. Goyal, Arijit Nath, Rasul Hafiz Ansar Suleria, Plant-Based Functional Foods and Phytochemicals, 2021
Arijit Nath, Titas Ghosh, Abinit Saha, Klára Pásztorné Huszár, Szilvia Bánvölgyi, Renáta Gerencsérné Berta, Ildikó Galambos, Edit Márki, Gyula Vatai, Andras Koris, Arpita Das
Antioxidants help to protect cells against oxidative stress. Free radicals (such as: reactive oxygen species-peroxides, superoxide, hydroxyl radical, singlet oxygen, and alpha-oxygen) and reactive nitrogen species (nitric oxide) as metabolic byproducts are produced due to unhealthy lifestyle, smoking, high alcohol consumption, over stress, inflammation, suffering with chronic metabolic disease. Their generation and accumulation are cause of oxidative damage of cell organelles, including DNA. Antioxidants operate by triggering and neutralizing free radicals in cell through (a) donating electron and (b) activation of transcription factor DAF-16 [5, 27].
Oxidative Stress and the Aging Brain: From Theory to Prevention
Published in David R. Riddle, Brain Aging, 2007
Carmelina Gemma, Jennifer Vila, Adam Bachstetter, Paula C. Bickford
There are a number of mutated genes that regulate the insulin/insulin growth factor 1 (IGF-1) signaling pathway. Age-1, daf-2, and daf-16 genes in C. elegans are associated with an insulin-like signaling pathway. Age-1 and daf-2 suppress the activity of the downstream target daf-16, a transcription factor that belongs to the Forkhead family of proteases [79]. Hence, loss of function of either of these upstream regulators enhances daf-16 function and leads to increased lifespan. Importantly, loss-of-function mutations in daf-16 not only prevents longevity conferred by the age-1 and daf-2 mutations, but also abolishes stress resistance [80], thereby strengthening the intimate link between longevity and the stress responsiveness associated pathway. These animals are smaller in size, and have a decreased body temperature and a modest increase in antioxidant capacity. Recent studies have shown that knockout mice for the IGF receptor live longer and display greater resistance to oxidative stress [81, 82].
Hibernation and Aging
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Cheng-Wei Wu, Kenneth B. Storey
Although it has been known for over a decade the positive role whereby FOXO confers longevity, the genes downstream of FOXO that are responsible for this phenotype remain largely elusive. A popular hypothesis is that FOXO mediates longevity by activating expression of genes involved in damage response to reactive oxygen species (ROS) such as super oxide dismutases (sod), forming an elevated protective system that limits cellular damage and increases life span. However, recent studies have shown that worms with deletion to all of its sod isoforms (sod-1 to 5) have a normal life span, and deletion mutations to the mitochondrial sod-2 isoform alone can actually increase longevity (Van Raamsdonk and Hekimi 2009, 2012). In C. elegans, knockdown of the DAF-16 protein alters the expression of over 3000 genes, these include regulation of genes involved in multiple stress responses (oxidative, heat, and pathogen), proteasome mediated protein degradation, lipid metabolism, and ribosome processing (Murphy et al. 2003). Although some of the downstream genes can mimic the longevity phenotypes of DAF-16, no single target gene alone can recapitulate the full effect of DAF-16 on life span, which upon deletion cause worms to be short-lived and abolishes the life span extension of the daf-2 mutants (Lin et al. 2001, Murphy et al. 2003). These studies have concluded that activation of DAF-16/FOXO likely functions to promote longevity by exerting the cell toward protections from a variety of extracellular stressors while promoting metabolic adjustments to optimize energy metabolism (Tullet 2015), forming a cellular environment much like the one established during hibernation.
Neuroprotective effects of rutin on ASH neurons in Caenorhabditis elegans model of Huntington’s disease
Published in Nutritional Neuroscience, 2022
Larissa Marafiga Cordeiro, Marcell Valandro Soares, Aline Franzen da Silva, Marina Lopes Machado, Fabiane Bicca Obetine Baptista, Tássia Limana da Silveira, Leticia Priscilla Arantes, Felix Alexandre Antunes Soares
The DAF-16 transcription factor, a C. elegans homolog of mammalian Forkhead box (FOXO), is thought to be the main target of DAF-2, an insulin/insulin-like growth factor (IGF)-1 receptor homolog [47]. Previous studies reported that DAF-16 plays a pivotal role in the regulation of longevity, and is also involved in the formation of less toxic, high-molecular-weight protein aggregates [48], via the activation of antioxidant genes and chaperones, thereby ameliorating polyQ aggregation and toxicity [49]. Our previous study demonstrated rutin-induced nuclear translocation of the DAF-16/FOXO transcription factor in C. elegans [7], which is essential for activating downstream genes. Under stress, DAF-16 proteins are phosphorylated and activated, and accumulate in the nucleus, thereby activating own functions to regulate downstream target genes, such as sod-3, which play an important role in metabolism, oxidative stress, and aging [50]. Genetic analysis has shown that DAF-16 is one of the essential transcriptional activators for a subset of chaperones, especially HSP-16.2. HSP-16.2 plays a protective role in polyQ diseases, as it promotes folding/refolding of proteins into appropriate conformations, and recovers previously aggregated proteins [51]. Molecular chaperones are also evolutionarily conserved in the cellular response to stress, and in the regulation of longevity, and some studies show a direct role of these components in the cellular stress response associated with the regulation of lifespan [52].
Detrimental effects of fructose on mitochondria in mouse motor neurons and on C. elegans healthspan
Published in Nutritional Neuroscience, 2022
Divya Lodha, Sudarshana Rajasekaran, Tamilselvan Jayavelu, Jamuna R. Subramaniam
Clarity is still sought after for the exact mechanisms by which fructose wreaks havoc. One of the direct mechanisms linked to mitochondria is the reduction of copper transporter, ctr-1, as shown in the stomach leading to Cu deficiency and high iron overload in rats fed on a high fructose diet31. As both Copper and iron are important components of the electron transport chain, it could directly impact the mitochondrial function. Another possibility is the generation of ROS13,14 and the absence of oxidative stress response. In vivo, in C. elegans, a high glucose/fructose diet abrogates all positive effects of the well – established reduced insulin signaling, brought about by mutations in the single exclusive Insulin/IGF-1 like receptor, daf-2, mediated 2 fold increase in lifespan with a proportionate increase in healthspan32. In daf-2 mutants, longevity is elicited through the removal of daf-2 mediated suppression of FOXO transcription factor, daf-16, and its downstream targets through the insulin/IGF-1 signaling cascade. Feeding glucose to daf-2 worms abrogates the longevity through downregulation of daf-16 and one of its targets, aquaporin, a glycerol channel, aqp-133. It needs to be established that fructose could be acting through the same mechanism.
Ilex paraguariensis extract provides increased resistance against oxidative stress and protection against Amyloid beta-induced toxicity compared to caffeine in Caenorhabditis elegans
Published in Nutritional Neuroscience, 2021
Marina Lopes Machado, Leticia Priscilla Arantes, Tássia Limana da Silveira, Daniele Coradini Zamberlan, Larissa Marafiga Cordeiro, Fabiane Baptista Bicca Obetine, Aline Franzen da Silva, Ivana Beatrice Mânica da Cruz, Felix Alexandre Antunes Soares, Riva de Paula Oliveira
DAF-16 and HSF-1 are two transcription factors regulated by insulin-like signaling [76]. DAF-16 and HSF-1 are involved in processes related to aging and antioxidant defenses [77] and heat shock protein expression and proteostasis, respectively [78,79]. Previous studies have reported that knocking down of DAF-2 (insulin-like receptor/IGF-1) reduced the levels of Aβ-induced toxicity in a DAF-16 and HSF-1 dependent manner [37]. Our results indicated that the IPHE-protective effect against body paralysis daf-6 and hsf-1(RNAi) failed to delay the onset of paralysis in CL2006 worms suggesting that DAF-16 and HSF-1 are required for the protective effect of IPHE and caffeine against Aβ1–42 toxicity. Taken together, these results suggested that IPHE and caffeine could protect against Aβ-induced toxicity by increasing the antioxidant defenses, expression of chaperonins and reducing the AChE activity and the expression of Aβ with the involvement of DAF-16 and HSF-1-dependent manner.