Sodium arsenite accelerates D-galactose-induced aging in the testis of the rat: Evidence for mitochondrial oxidative damage, NF-kB, JNK, and apoptosis pathways

Akbari, Sholeh; Seyedabadi, Mohammad; Amiri, Fereshteh Talebpour; Naderi, Maloos; Shaki, Fatemeh

doi:10.1016/j.tox.2022.153148

Cited by 16 publications

(9 citation statements)

References 88 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, as reprogramming somatic cells into iPSCs coincides with cellular rejuvenation, our MN model could well be recapitulating young MNs, while ALS(6) symptoms typically present later in life. To model age-associated damage, we therefore added an oxidative stress component to our model system by exposing the cells to sodium arsenite (SA) (Akbari et al, 2022; Baron et al, 2013). Furthermore, increased oxidative stress and ROS accumulation has been extensively reported as a hallmark of ALS as ROS are byproducts of cellular respiration as neurons have higher metabolic rates and transcriptional activity (Vandoorne et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

IFNγ protects motor neurons from oxidative stress via enhanced global protein synthesis in FUS-associated Amyotrophic Lateral Sclerosis

Assoni

Guerrero

Wardenaar

et al. 2022

Preprint

View full text Add to dashboard Cite

Amyotrophic lateral sclerosis type 6 (ALS6) is a familial subtype of ALS linked to Fused in Sarcoma (FUS) gene mutation.FUSmutations lead to decreased global protein synthesis, but the mechanism that drives this has not been established. Here, we used ALS6 patient-derived induced pluripotent stem cells (hIPSCs) to study the effect of the ALS6 FUSR521H mutation on the translation machinery in motor neurons (MNs). We find, in agreement with findings of others, that protein synthesis is decreased in ALS6 MNs. Furthermore, ALS6 MNs are more sensitive to oxidative stress and display reduced expression of TGF-β and mTORC gene pathways when stressed. Finally, we show that IFNγ treatment reduces apoptosis of ALS6 MNs exposed to oxidative stress and partially restores the translation rates in ALS6 MNs. Overall, these findings suggest that a functional IFNγ response is important for FUS-mediated protein synthesis, possibly by FUS nuclear translocation in ALS6.

show abstract

Section: Discussionmentioning

confidence: 99%

IFNγ protects motor neurons from oxidative stress via enhanced global protein synthesis in FUS-associated Amyotrophic Lateral Sclerosis

Assoni

Guerrero

Wardenaar

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Epigenetic changes (Yatsenko and Turek, 2018;Zambrano et al, 2021) Inappropriate redox balance (Beattie et al, 2015;Weir and Robaire, 2007) Decreased UPR-related proteins (Cavalcante et al, 2020;Zhao et al, 2019) Apoptosis (Akbari et al, 2022;Zhao et al, 2019) decline in oocyte quality and quantity is multifactorial and is poorly understood. One of the most central determinants of oocyte quality is chromosome segregation during meiosis.…”

Section: The Molecular Mechanisms Underlying Age-associatedmentioning

confidence: 99%

The landscape of aging

Cai

Song

et al. 2022

Sci. China Life Sci.

201

View full text Add to dashboard Cite

Aging is characterized by a progressive deterioration of physiological integrity, leading to impaired functional ability and ultimately increased susceptibility to death. It is a major risk factor for chronic human diseases, including cardiovascular disease, diabetes, neurological degeneration, and cancer. Therefore, the growing emphasis on “healthy aging” raises a series of important questions in life and social sciences. In recent years, there has been unprecedented progress in aging research, particularly the discovery that the rate of aging is at least partly controlled by evolutionarily conserved genetic pathways and biological processes. In an attempt to bring full-fledged understanding to both the aging process and age-associated diseases, we review the descriptive, conceptual, and interventive aspects of the landscape of aging composed of a number of layers at the cellular, tissue, organ, organ system, and organismal levels.

show abstract

“…However, it has been well established and accepted by the scientific community that a disrupted antioxidant/oxidant equilibrium coupled with an accumulation of oxidative damage to cellular constituents (DNA, proteins, lipids) and a chronic inflammation are pervasive features of ageing [ 42 , 43 ]. Key inflammatory players are indeed involved in the age-related process: activation of the pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, upregulation of cytokines (interleukin 1 beta (IL-1β), IL-6, tumour necrosis factor alpha (TNF-α)), C-C motif chemokine ligands (CCL2, CCL20) and their receptors, and other proinflammatory factors (matrix metalloproteinases, COX2, and NOS2) [ 42 , 44 , 45 , 46 , 47 , 48 ]. All these pro-inflammatory actors are indeed more expressed in aged than in young tissues [ 44 , 49 ].…”

Section: Beneficial and Harmful Roles Of Rosmentioning

confidence: 99%

Normal and Pathological NRF2 Signalling in the Central Nervous System

et al. 2022

View full text Add to dashboard Cite

The nuclear factor erythroid 2-related factor 2 (NRF2) was originally described as a master regulator of antioxidant cellular response, but in the time since, numerous important biological functions linked to cell survival, cellular detoxification, metabolism, autophagy, proteostasis, inflammation, immunity, and differentiation have been attributed to this pleiotropic transcription factor that regulates hundreds of genes. After 40 years of in-depth research and key discoveries, NRF2 is now at the center of a vast regulatory network, revealing NRF2 signalling as increasingly complex. It is widely recognized that reactive oxygen species (ROS) play a key role in human physiological and pathological processes such as ageing, obesity, diabetes, cancer, and neurodegenerative diseases. The high oxygen consumption associated with high levels of free iron and oxidizable unsaturated lipids make the brain particularly vulnerable to oxidative stress. A good stability of NRF2 activity is thus crucial to maintain the redox balance and therefore brain homeostasis. In this review, we have gathered recent data about the contribution of the NRF2 pathway in the healthy brain as well as during metabolic diseases, cancer, ageing, and ageing-related neurodegenerative diseases. We also discuss promising therapeutic strategies and the need for better understanding of cell-type-specific functions of NRF2 in these different fields.

show abstract

Sodium arsenite accelerates D-galactose-induced aging in the testis of the rat: Evidence for mitochondrial oxidative damage, NF-kB, JNK, and apoptosis pathways

Cited by 16 publications

References 88 publications

IFNγ protects motor neurons from oxidative stress via enhanced global protein synthesis in FUS-associated Amyotrophic Lateral Sclerosis

IFNγ protects motor neurons from oxidative stress via enhanced global protein synthesis in FUS-associated Amyotrophic Lateral Sclerosis

The landscape of aging

Normal and Pathological NRF2 Signalling in the Central Nervous System

Contact Info

Product

Resources

About