scholarly journals A brief review on cigarette induced cellular damage

2020 ◽  
Vol 23 ◽  
pp. 18-25
Author(s):  
Sudip Dey ◽  
◽  
Pokhraj Guha
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoking ◽  
Tobacco Consumption ◽  
Cellular Damage ◽  
Immunoglobulin Level ◽  
Serum Immunoglobulin Level ◽  
Unfolded Protein ◽  
Chronic Oxidative Stress ◽  
Long Time ◽  
Protein Response

Cigarette smoking has become one of the most common addictions in context to the present scenario of tobacco consumption. Comprising of nearly 7000 chemicals, cigarette smoke have both free radicals and oxidizing agents in both smoke tar and gas phase, both of which can cause oxidative stress in human health. Long time smoking causes decreased serum immunoglobulin level but increased level of auto– antibodies. During chronic oxidative stress resulting from cigarette smoking, cells secrete mucus and increased viscosity of mucus in airways makes it susceptible to bacterial infection. Furthermore, chronic exposure of lungs to tobacco smoke causes unfolded protein response, ER stress and altered ceramide metabolism. Apart from the above mentioned facts, Cigarette smoking can also cause senescence resulting in abnormal wound healing that exaggerates pathogenesis of COPD. Although there are several management therapies available for COPD management, but the permanent cellular damages due to smoking are irreparable and results in disease exaggeration and suffering.

The biochemistry and cell biology of aging: metabolic regulation through mitochondrial signaling

2014 ◽  
Vol 306 (6) ◽  
pp. E581-E591 ◽  
Author(s):  
Yun Chau Long ◽  
Theresa May Chin Tan ◽  
Inoue Takao ◽  
Bor Luen Tang
Keyword(s):  
Cell Biology ◽  
Metabolic Regulation ◽  
Nutrient Sensing ◽  
Cellular Aging ◽  
Retrograde Signaling ◽  
Unfolded Protein ◽  
Mitochondrial Retrograde Signaling ◽  
Long Time ◽  
Biology Of Aging ◽  
Protein Response

Cellular and organ metabolism affects organismal lifespan. Aging is characterized by increased risks for metabolic disorders, with age-associated degenerative diseases exhibiting varying degrees of mitochondrial dysfunction. The traditional view of the role of mitochondria generated reactive oxygen species (ROS) in cellular aging, assumed to be causative and simply detrimental for a long time now, is in need of reassessment. While there is little doubt that high levels of ROS are detrimental, mounting evidence points toward a lifespan extension effect exerted by mild to moderate ROS elevation. Dietary caloric restriction, inhibition of insulin-like growth factor-I signaling, and inhibition of the nutrient-sensing mechanistic target of rapamycin are robust longevity-promoting interventions. All of these appear to elicit mitochondrial retrograde signaling processes (defined as signaling from the mitochondria to the rest of the cell, for example, the mitochondrial unfolded protein response, or UPRmt). The effects of mitochondrial retrograde signaling may even spread to other cells/tissues in a noncell autonomous manner by yet unidentified signaling mediators. Multiple recent publications support the notion that an evolutionarily conserved, mitochondria-initiated signaling is central to the genetic and epigenetic regulation of cellular aging and organismal lifespan.

scholarly journals Effect of liposome-encapsulated hemoglobin resuscitation on proteostasis in small intestinal epithelium after hemorrhagic shock

2016 ◽  
Vol 311 (1) ◽  
pp. G180-G191 ◽  
Author(s):  
Geeta Rao ◽  
Vivek R. Yadav ◽  
Shanjana Awasthi ◽  
Pamela R. Roberts ◽  
Vibhudutta Awasthi
Keyword(s):  
Oxidative Stress ◽  
Hemorrhagic Shock ◽  
Multiorgan Failure ◽  
Sprague Dawley ◽  
Barrier Dysfunction ◽  
Protective Mechanisms ◽  
Unfolded Protein ◽  
Sprague Dawley Rats ◽  
Markers Of Oxidative Stress ◽  
Protein Response

Gut barrier dysfunction is the major trigger for multiorgan failure associated with hemorrhagic shock (HS). Although the molecular mediators responsible for this dysfunction are unclear, oxidative stress-induced disruption of proteostasis contributes to the gut pathology in HS. The objective of this study was to investigate whether resuscitation with nanoparticulate liposome-encapsulated hemoglobin (LEH) is able to restore the gut proteostatic mechanisms. Sprague-Dawley rats were recruited in four groups: control, HS, HS+LEH, and HS+saline. HS was induced by withdrawing 45% blood, and isovolemic LEH or saline was administered after 15 min of shock. The rats were euthanized at 6 h to collect plasma and ileum for measurement of the markers of oxidative stress, unfolded protein response (UPR), proteasome function, and autophagy. HS significantly increased the protein and lipid oxidation, trypsin-like proteasome activity, and plasma levels of IFNγ. These effects were prevented by LEH resuscitation. However, saline was not able to reduce protein oxidation and plasma IFNγ in hemorrhaged rats. Saline resuscitation also suppressed the markers of UPR and autophagy below the basal levels; the HS or LEH groups showed no effect on the UPR and autophagy. Histological analysis showed that LEH resuscitation significantly increased the villus height and thickness of the submucosal and muscularis layers compared with the HS and saline groups. Overall, the results showed that LEH resuscitation was effective in normalizing the indicators of proteostasis stress in ileal tissue. On the other hand, saline-resuscitated animals showed a decoupling of oxidative stress and cellular protective mechanisms.

Causal role of oxidative stress in unfolded protein response development in the hyperthyroid state

2015 ◽  
Vol 89 ◽  
pp. 401-408 ◽  
Author(s):  
Luis A. Videla ◽  
Virginia Fernández ◽  
Pamela Cornejo ◽  
Romina Vargas ◽  
Juan Carrasco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Unfolded Protein Response ◽  
Causal Role ◽  
Unfolded Protein ◽  
Hyperthyroid State ◽  
Protein Response

scholarly journals Phenolic Compounds Reduce the Fat Content in Caenorhabditis elegans by Affecting Lipogenesis, Lipolysis, and Different Stress Responses

2020 ◽  
Vol 13 (11) ◽  
pp. 355
Author(s):  
Paula Aranaz ◽  
David Navarro-Herrera ◽  
María Zabala ◽  
Ana Romo-Hualde ◽  
Miguel López-Yoldi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Phenolic Compounds ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Lipid Mobilization ◽  
C Elegans ◽  
Unfolded Protein ◽  
Reducing Activity ◽  
Protein Response

Supplementation with bioactive compounds capable of regulating energy homeostasis is a promising strategy to manage obesity. Here, we have screened the ability of different phenolic compounds (myricetin, kaempferol, naringin, hesperidin, apigenin, luteolin, resveratrol, curcumin, and epicatechin) and phenolic acids (p-coumaric, ellagic, ferulic, gallic, and vanillic acids) regulating C. elegans fat accumulation. Resveratrol exhibited the strongest lipid-reducing activity, which was accompanied by the improvement of lifespan, oxidative stress, and aging, without affecting worm development. Whole-genome expression microarrays demonstrated that resveratrol affected fat mobilization, fatty acid metabolism, and unfolded protein response of the endoplasmic reticulum (UPRER), mimicking the response to calorie restriction. Apigenin induced the oxidative stress response and lipid mobilization, while vanillic acid affected the unfolded-protein response in ER. In summary, our data demonstrates that phenolic compounds exert a lipid-reducing activity in C. elegans through different biological processes and signaling pathways, including those related with lipid mobilization and fatty acid metabolism, oxidative stress, aging, and UPR-ER response. These findings open the door to the possibility of combining them in order to achieve complementary activity against obesity-related disorders.

scholarly journals Fine Particulate Matter Leads to Unfolded Protein Response and Shortened Lifespan by Inducing Oxidative Stress in C. elegans

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Yunli Zhao ◽  
Ling Jin ◽  
Yuxin Chi ◽  
Jing Yang ◽  
Quan Zhen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Metabolic Enzyme ◽  
C Elegans ◽  
Unfolded Protein ◽  
Fine Particulate ◽  
Underlying Mechanisms ◽  
Protein Response ◽  
Phenylbutyric Acid

Oxidative stress has been proven as one of the most critical regulatory mechanisms involved in fine Particulate Matter- (PM2.5-) mediated toxicity. For a better understanding of the underlying mechanisms that enable oxidative stress to participate in PM2.5-induced toxic effects, the current study explored the effects of oxidative stress induced by PM2.5 on UPR and lifespan in C. elegans. The results implicated that PM2.5 exposure induced oxidative stress response, enhanced metabolic enzyme activity, activated UPR, and shortened the lifespan of C. elegans. Antioxidant N-acetylcysteine (NAC) could suppress the UPR through reducing the oxidative stress; both the antioxidant NAC and UPR inhibitor 4-phenylbutyric acid (4-PBA) could rescue the lifespan attenuation caused by PM2.5, indicating that the antioxidant and moderate proteostasis contribute to the homeostasis and adaptation to oxidative stress induced by PM2.5.

scholarly journals Suppression of Mouse AApoAII Amyloidosis Progression by Daily Supplementation with Oxidative Stress Inhibitors

2019 ◽  
Vol 2019 ◽  
pp. 1-14
Author(s):  
Jian Dai ◽  
Xin Ding ◽  
Hiroki Miyahara ◽  
Zhe Xu ◽  
Xiaoran Cui ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Misfolding ◽  
Amyloid Fibrils ◽  
Treatment Strategies ◽  
Amyloid Deposition ◽  
Unfolded Protein ◽  
Antioxidative Effects ◽  
The Unfolded Protein Response ◽  
Protein Response ◽  
Protein Misfolding And Aggregation

Amyloidosis is a group of diseases characterized by protein misfolding and aggregation to form amyloid fibrils and subsequent deposition within various tissues. Previous studies have indicated that amyloidosis is often associated with oxidative stress. However, it is not clear whether oxidative stress is involved in the progression of amyloidosis. We administered the oxidative stress inhibitors tempol and apocynin via drinking water to the R1.P1-Apoa2c mouse strain induced to develop mouse apolipoprotein A-II (AApoAII) amyloidosis and found that treatment with oxidative stress inhibitors led to reduction in AApoAII amyloidosis progression compared to an untreated group after 12 weeks, especially in the skin, stomach, and liver. There was no effect on ApoA-II plasma levels or expression of Apoa2 mRNA. Detection of the lipid peroxidation markers 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA) revealed that the antioxidative effects of the treatments were most obvious in the skin, stomach, and liver, which contained higher levels of basal oxidative stress. Moreover, the unfolded protein response was reduced in the liver and was associated with a decrease in oxidative stress and amyloid deposition. These results suggest that antioxidants can suppress the progression of AApoAII amyloid deposition in the improved microenvironment of tissues and that the effect may be related to the levels of oxidative stress in local tissues. This finding provides insights for antioxidative stress treatment strategies for amyloidosis.

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