scholarly journals MHC genes and oxidative stress in sticklebacks: an immuno-ecological approach

2006 ◽  
Vol 273 (1592) ◽  
pp. 1407-1414 ◽  
Author(s):  
Joachim Kurtz ◽  
K. Mathias Wegner ◽  
Martin Kalbe ◽  
Thorsten B.H Reusch ◽  
Helmut Schaschl ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Susceptibility To Infection ◽  
Mhc Genes ◽  
Histocompatibility Complex ◽  
Individual Host ◽  
Experimental Approaches ◽  
Mhc Class Iib ◽  
Class Iib ◽  
First Time ◽  
And Oxidative Stress

Individual variation in the susceptibility to infection may result from the varying ability of hosts to specifically recognize different parasite strains. Alternatively, there could be individual host differences in fitness costs of immune defence. Although, these two explanations are not mutually exclusive, they have so far been treated in separate experimental approaches. To analyse potential relationships, we studied body condition and oxidative stress, which may reflect costs of immunity, in three-spined sticklebacks that had been experimentally exposed to three species of naturally occurring parasite. These sticklebacks differed in a trait, which is crucial to specific parasite defence, i.e. individual genetic diversity at major histocompatibility complex (MHC) class IIB loci. Oxidative stress was quantified as tissue acrolein, a technique that has been applied to questions of immuno-ecology for the first time. We measured gene expression at the MHC and other estimates of immune activation. We found that fish with high levels of MHC expression had poor condition and elevated oxidative stress. These results indicate that MHC-based specific immunity is connected with oxidative stress. They could, thus, also be relevant in the broader context of the evolution of sexually selected signals that are based on carotenoids and are, thus supposed to reflect oxidative stress resistance.

scholarly journals Chronic Exposure to Water-Pipe Smoke Induces Alveolar Enlargement, DNA Damage and Impairment of Lung Function

2016 ◽  
Vol 38 (3) ◽  
pp. 982-992 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Javed Yasin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Lung Function ◽  
Respiratory System ◽  
Lung Inflammation ◽  
Experimental Studies ◽  
Damage Index ◽  
Water Pipe ◽  
First Time ◽  
And Oxidative Stress

Background/Aim: Epidemiological evidence indicates that water-pipe smoking (WPS) adversely affects the respiratory system. However, the mechanisms underlying its effects are not well understood. Recent experimental studies reported the occurrence of lung inflammation and oxidative stress following acute and subacute exposure to WPS. Here, we wanted to verify the extent of inflammation and oxidative stress in mice chronically-exposed to WPS and to evaluate, for the first time, its effect on alveolar injury and DNA damage and their association with impairment of lung function. Methods: Mice were nose-only exposed to mainstream WPS (30 min/day; 5 days/week for 6 consecutive months). Control mice were exposed using the same protocol to atmospheric air only. At the end of the exposure period, several respiratory parameters were assessed. Results: In bronchoalveolar lavage fluid, WPS increased neutrophil and lymphocyte numbers, lactate dehydrogenase, myeloperoxidase and matrix metallopeptidase 9 activities, as well as several proinflammatory cytokines. In lung tissue, lipid peroxidation, reactive oxygen species, superoxide dismutase activity and reduced glutathione were all increased by WPS exposure. Along with oxidative stress, WPS exposure significantly increased lung DNA damage index. Histologically the lungs of WPS-exposed mice had foci of mixed inflammatory cells infiltration in the interalveolar interstitium which consisted of neutrophils, lymphocytes and macrophages. Interestingly, we found dilated alveolar spaces and alveolar ducts with damaged interalveolar septae, and impairment of lung function following WPS exposure. Conclusion: We show the persistence of lung inflammation and oxidative stress in mice chronically-exposed to WPS and demonstrate, for the first time, the occurrence of DNA damage and enlargement of alveolar spaces and ducts associated with impairment of lung function. Our findings provide novel mechanistic elucidation for the long-term effects of WPS on the respiratory system.

scholarly journals The Universal Soldier: Enzymatic and Non-Enzymatic Antioxidant Functions of Serum Albumin

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 966
Author(s):  
Daria A. Belinskaia ◽  
Polina A. Voronina ◽  
Vladimir I. Shmurak ◽  
Mikhail A. Vovk ◽  
Anastasia A. Batalova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Serum Albumin ◽  
Antioxidant Properties ◽  
Redox Status ◽  
Allosteric Modulation ◽  
Biologically Active ◽  
Redox Modulation ◽  
Antioxidant Defence ◽  
First Time ◽  
And Oxidative Stress

As a carrier of many biologically active compounds, blood is exposed to oxidants to a greater extent than the intracellular environment. Serum albumin plays a key role in antioxidant defence under both normal and oxidative stress conditions. This review evaluates data published in the literature and from our own research on the mechanisms of the enzymatic and non-enzymatic activities of albumin that determine its participation in redox modulation of plasma and intercellular fluid. For the first time, the results of numerous clinical, biochemical, spectroscopic and computational experiments devoted to the study of allosteric modulation of the functional properties of the protein associated with its participation in antioxidant defence are analysed. It has been concluded that it is fundamentally possible to regulate the antioxidant properties of albumin with various ligands, and the binding and/or enzymatic features of the protein by changing its redox status. The perspectives for using the antioxidant properties of albumin in practice are discussed.

scholarly journals Effects of the Quinone Oxidoreductase WrbA on Escherichia coli Biofilm Formation and Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 919
Author(s):  
Federico Rossi ◽  
Cristina Cattò ◽  
Gianmarco Mugnai ◽  
Federica Villa ◽  
Fabio Forlani
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Biofilm Formation ◽  
Cinnamic Acids ◽  
Quinone Oxidoreductase ◽  
Oxidoreductase Activity ◽  
Biofilm Thickness ◽  
Biofilm Development ◽  
First Time ◽  
And Oxidative Stress

The effects of natural compounds on biofilm formation have been extensively studied, with the goal of identifying biofilm formation antagonists at sub-lethal concentrations. Salicylic and cinnamic acids are some examples of these compounds that interact with the quinone oxidoreductase WrbA, a potential biofilm modulator and an antibiofilm compound biomarker. However, WrbA’s role in biofilm development is still poorly understood. To investigate the key roles of WrbA in biofilm maturation and oxidative stress, Escherichia coli wild-type and ∆wrbA mutant strains were used. Furthermore, we reported the functional validation of WrbA as a molecular target of salicylic and cinnamic acids. The lack of WrbA did not impair planktonic growth, but rather affected the biofilm formation through a mechanism that depends on reactive oxygen species (ROS). The loss of WrbA function resulted in an ROS-sensitive phenotype that showed reductions in biofilm-dwelling cells, biofilm thickness, matrix polysaccharide content, and H2O2 tolerance. Endogenous oxidative events in the mutant strain generated a stressful condition to which the bacterium responded by increasing the catalase activity to compensate for the lack of WrbA. Cinnamic and salicylic acids inhibited the quinone oxidoreductase activity of purified recombinant WrbA. The effects of these antibiofilm molecules on WrbA function was proven for the first time.

scholarly journals Mitochondrial dysfunction promotes alternative gasdermin D-mediated inflammatory cell death and susceptibility to infection

2021 ◽  
Author(s):  
Chi G Weindel ◽  
Xiao Zhao ◽  
Eduardo Martinez ◽  
Samantha L Bell ◽  
Krystal J Vail ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Mycobacterium Tuberculosis ◽  
Inflammatory Cell ◽  
Inflammatory Diseases ◽  
Neutrophil Infiltration ◽  
Inflammasome Activation ◽  
Leucine Rich Repeat ◽  
Susceptibility To Infection ◽  
And Oxidative Stress

Human mutations in mitochondrial-associated genes are associated with inflammatory diseases and susceptibility to infection. However, their mechanistic contributions to immune outcomes remain ill-defined. We discovered that the disease-associated gain-of-function allele Lrrk2G2019S (leucine-rich repeat kinase 2) promotes mitochondrial hyper-fission, depolarization, and oxidative stress in macrophages. In the presence of Lrrk2G2019S-dependent mitochondrial perturbations, AIM2 inflammasome activation promotes more cell death but not more pyroptotic IL-1β release. Instead, inflammasome activation in Lrrk2G2019S macrophages triggers gasdermin D (GSDMD)-mediated mitochondrial pores, driving up ROS-mediated RIPK1/RIPK3/MLKL dependent necroptosis. Consequently, infection of Lrrk2G2019S mice with Mycobacterium tuberculosis elicits hyperinflammation and immunopathology via enhanced neutrophil infiltration. By uncovering that GSDMD promotes non-pyroptotic cell death in Lrrk2G2019S macrophages, our findings demonstrate that altered mitochondrial function can reprogram cell death modalities to elicit distinct immune outcomes. This provides mechanistic insights into why mutations in LRRK2 are associated with susceptibility to chronic inflammatory and infectious diseases.

scholarly journals Mitochondria’s Role in Skin Ageing

Biology ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 29 ◽  
Author(s):  
Roisin Stout ◽  
Mark Birch-Machin
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Barrier Function ◽  
External Factors ◽  
Susceptibility To Infection ◽  
Skin Cells ◽  
Key Features ◽  
Skin Function ◽  
Skin Care Products ◽  
And Oxidative Stress

Skin ageing is the result of a loss of cellular function, which can be further accelerated by external factors. Mitochondria have important roles in skin function, and mitochondrial damage has been found to accumulate with age in skin cells, but also in response to solar light and pollution. There is increasing evidence that mitochondrial dysfunction and oxidative stress are key features in all ageing tissues, including skin. This is directly linked to skin ageing phenotypes: wrinkle formation, hair greying and loss, uneven pigmentation and decreased wound healing. The loss of barrier function during skin ageing increases susceptibility to infection and affects wound healing. Therefore, an understanding of the mechanisms involved is important clinically and also for the development of antiageing skin care products.

scholarly journals Odour-based discrimination of similarity at the major histocompatibility complex in birds

2017 ◽  
Vol 284 (1846) ◽  
pp. 20162466 ◽  
Author(s):  
Sarah Leclaire ◽  
Maria Strandh ◽  
Jérôme Mardon ◽  
Helena Westerdahl ◽  
Francesco Bonadonna
Keyword(s):  
Major Histocompatibility Complex ◽  
High Throughput Sequencing ◽  
Choice Test ◽  
Antigen Binding ◽  
Mating Pattern ◽  
Major Histocompatibility ◽  
Good Sense ◽  
Histocompatibility Complex ◽  
Mhc Class Iib ◽  
Class Iib

Many animals are known to preferentially mate with partners that are dissimilar at the major histocompatibility complex (MHC) in order to maximize the antigen binding repertoire (or disease resistance) in their offspring. Although several mammals, fish or lizards use odour cues to assess MHC similarity with potential partners, the ability of birds to assess MHC similarity using olfactory cues has not yet been explored. Here we used a behavioural binary choice test and high-throughput-sequencing of MHC class IIB to determine whether blue petrels can discriminate MHC similarity based on odour cues alone. Blue petrels are seabirds with particularly good sense of smell, they have a reciprocal mate choice and are known to preferentially mate with MHC-dissimilar partners. Incubating males preferentially approached the odour of the more MHC-dissimilar female, whereas incubating females showed opposite preferences. Given their mating pattern, females were, however, expected to show preference for the odour of the more MHC-dissimilar male. Further studies are needed to determine whether, as in women and female mice, the preference varies with the reproductive cycle in blue petrel females. Our results provide the first evidence that birds can use odour cues only to assess MHC dissimilarity.

scholarly journals A novel SOD1-dependent mechanism for the iron-induced production of toxic SOD1 and oxidative stress that initiates ALS

2015 ◽  
Author(s):  
Liang Zhong Lim ◽  
Jianxing Song
Keyword(s):  
Oxidative Stress ◽  
Wild Type ◽  
Motor Neuron Degeneration ◽  
Neuron Degeneration ◽  
Fenton Chemistry ◽  
Cuzn Superoxide Dismutase ◽  
Blood Spinal Cord Barrier ◽  
First Time ◽  
And Oxidative Stress ◽  
Dependent Mechanism

Free iron is highly toxic and the blood-derived iron initiates early motor-neuron degeneration upon breakdown of blood-spinal cord barrier. Iron is currently known to trigger oxidative stress by Fenton chemistry but no report implies that iron manifests its toxicity through CuZn-superoxide dismutase (SOD1), the central antioxidant enzyme in all human tissues that carries >180 ALS-causing mutations. Here, by NMR we show that Zn2+ play an irreplaceable role in the maturation of the nascent hSOD1, and further decipher for the first time that out of 11 other cations only Fe2+ has the Zn2+-like capacity to induce folding to form the Fe2+-bound hSOD1. This acts to reduce or even block the maturation of wild-type and ALS-causing mutant hSOD1, consequently trapping SOD1 in toxic forms and provoking oxidative stress. Our study establishes a novel SOD1-dependent mechanism for iron to manifest cellular toxicity that contributes to pathogenesis of neurodegenerative diseases, aging and even more.

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