Pathophysiological effects of cadmium(II) on human health-a critical review

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Kaustav Bhattacharyya ◽  
Debrup Sen ◽  
Payel Laskar ◽  
Tania Saha ◽  
Gautam Kundu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endocrine Disruption ◽  
Cell Signalling ◽  
Dna Lesions ◽  
Anthropogenic Sources ◽  
Oxygen Species ◽  
Cellular Biochemistry ◽  
Contaminated Food ◽  
Industrial Sources ◽  
Potent Carcinogen

Abstract Cadmium(II) is an omnipresent environmental toxicant emitted from various industrial sources and by anthropogenic sources such as smoking. Cadmium(II) enters our body through various sources including contaminated food and drinks and from active or passive smoking. It spares no organs in our body and the calamities it invites include primarily nephrotoxicity, osteotoxicity, teratogenicity, endocrine disruption, hepatotoxicity and carcinogenicity above all. It brings about a bolt from the blue in the cellular biochemistry by generating reactive oxygen species (ROS), disrupting the factors involved in the repair of DNA lesions and many other toxic nuisances otherwise by modulating the cell signalling machinery and acting as a potent carcinogen above all. In this review, we have tried to decipher some of the mechanisms played by cadmium(II) in exhibiting its toxic effects on various system of our body.

Subversion of host cell signalling by the protozoan parasiteLeishmania

Parasitology ◽  
2005 ◽  
Vol 130 (S1) ◽  
pp. S27-S35 ◽  
Author(s):  
D. J. GREGORY ◽  
M. OLIVIER
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cell Signalling ◽  
Protein Tyrosine Phosphatases ◽  
Innate Immune ◽  
Signalling Pathways ◽  
Oxygen Species ◽  
Obligate Intracellular ◽  
Intracellular Parasites ◽  
Intracellular Ca

The protozoaLeishmaniaspp. are obligate intracellular parasites that inhabit the macrophages of their host. Since macrophages are specialized for the identification and destruction of invading pathogens, both directly and by triggering an innate immune response,Leishmaniahave evolved a number of mechanisms for suppressing some critical macrophage activities. In this review, we discuss how various species ofLeishmaniadistort the host macrophage's own signalling pathways to repress the expression of various cytokines and microbicidal molecules (nitric oxide and reactive oxygen species), and antigen presentation. In particular, we describe how MAP Kinase and JAK/STAT cascades are repressed, and intracellular Ca2+and the activities of protein tyrosine phosphatases, in particular SHP-1, are elevated.

Cell signalling by oxidized lipids and the role of reactive oxygen species in the endothelium

2005 ◽  
Vol 33 (6) ◽  
pp. 1385-1389 ◽  
Author(s):  
J.W. Zmijewski ◽  
A. Landar ◽  
N. Watanabe ◽  
D.A. Dickinson ◽  
N. Noguchi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Oxidation ◽  
Protein Function ◽  
Cell Signalling ◽  
Reactive Oxygen ◽  
Oxidation Products ◽  
Oxidized Lipids ◽  
Oxygen Species ◽  
Post Translational Modification ◽  
Lipid Oxidation Products

The controlled formation of ROS (reactive oxygen species) and RNS (reactive nitrogen species) is now known to be critical in cellular redox signalling. As with the more familiar phosphorylation-dependent signal transduction pathways, control of protein function is mediated by the post-translational modification at specific amino acid residues, notably thiols. Two important classes of oxidant-derived signalling molecules are the lipid oxidation products, including those with electrophilic reactive centres, and decomposition products such as lysoPC (lysophosphatidylcholine). The mechanisms can be direct in the case of electrophiles, as they can modify signalling proteins by post-translational modification of thiols. In the case of lysoPC, it appears that secondary generation of ROS/RNS, dependent on intracellular calcium fluxes, can cause the secondary induction of H2O2 in the cell. In either case, the intracellular source of ROS/RNS has not been defined. In this respect, the mitochondrion is particularly interesting since it is now becoming apparent that the formation of superoxide from the respiratory chain can play an important role in cell signalling, and oxidized lipids can stimulate ROS formation from an undefined source. In this short overview, we describe recent experiments that suggest that the cell signalling mediated by lipid oxidation products involves their interaction with mitochondria. The implications of these results for our understanding of adaptation and the response to stress in cardiovascular disease are discussed.

scholarly journals Predominance of Secondary Organic Aerosol to Particle-bound Reactive Oxygen Species Activity in Fine Ambient Aerosol

2019 ◽  
Author(s):  
Jun Zhou ◽  
Miriam Elser ◽  
Ru-Jin Huang ◽  
Manuel Krapf ◽  
Roman Fröhlich ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Health Effects ◽  
Secondary Organic Aerosol ◽  
Reactive Oxygen ◽  
Organic Aerosol ◽  
Epidemiological Studies ◽  
Anthropogenic Sources ◽  
Emission Sources ◽  
Oxygen Species ◽  
Concentration Variance

Abstract. Reactive oxygen species (ROS) are believed to contribute to the adverse health effects of aerosols. This may happen by inhaled particle-bound (exogenic) ROS (PB-ROS) or by ROS formed within the respiratory tract by certain aerosol components (endogenic ROS). We investigated the chemical composition of aerosols and their exogenic ROS content at the two contrasting locations Beijing (China) and Bern (Switzerland). We apportioned the ambient organic aerosol to different sources and attributed the observed PB-ROS to them. The oxygenated organic aerosol (OOA, a proxy for secondary organic aerosol, SOA) explained the highest fraction of the exogenic ROS concentration variance at both locations. We also characterized primary and secondary aerosol emissions generated from different biogenic and anthropogenic sources in smog chamber experiments. The exogenic PB-ROS content in the OOA from these emission sources was comparable to that in the ambient measurements. Our results imply that SOA from gaseous precursors of different anthropogenic emission sources is a crucial source of PB-ROS and should be additionally considered in toxicological and epidemiological studies in an adequate way besides primary emissions. The importance of PB-ROS may be connected to the seasonal trends in health effects of PM reported by epidemiological studies, with elevated incidences of adverse effects in warmer seasons, which are accompanied by more intense atmospheric oxidation processes.

scholarly journals Oxidative stress in marathon runners: interest of antioxidant supplementation

2006 ◽  
Vol 96 (S1) ◽  
pp. S31-S33 ◽  
Author(s):  
Mari-Carmen Gomez-Cabrera ◽  
Agustín Martínez ◽  
Gustavo Santangelo ◽  
Federico V. Pallardó ◽  
Juan Sastre ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Cell Signalling ◽  
Reactive Oxygen ◽  
Peripheral Blood Lymphocytes ◽  
Signalling Pathways ◽  
Marathon Running ◽  
Oxygen Species ◽  
Marathon Runners

We have recently reported that xanthine oxidase is involved in the generation of free radicals in exhaustive exercise. Allopurinol, an inhibitor of xanthine oxidase, prevents it. The aim of the present work was to elucidate the role of exercise-derived reactive oxygen species in the cell signalling pathways involved in the adaptation to exercise in man. We have found that exercise causes an increase in the activity of plasma xanthine oxidase and an activation of NF-κB in peripheral blood lymphocytes after marathon running. This activation is dependent on free radical formation in exercise: treatment with allopurinol completely prevents it. In animal models, we previously showed that NF-κB activation induced by exhaustive physical exercise leads to an increase in the expression of superoxide dismutase, an enzyme involved in antioxidant defence. We report evidence in man that reactive oxygen species act as signals in exercise as decreasing their formation prevents activation of important signalling pathways which can cause useful adaptations in cells.

scholarly journals Site-specific targeting of a light activated dCas9-KIllerRed fusion protein generates transient, localized regions of oxidative DNA damage

2020 ◽  
Author(s):  
Nealia C.M. House ◽  
Jacob V. Layer ◽  
Brendan D. Price
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Light Exposure ◽  
Green Light ◽  
Reactive Oxygen ◽  
Dna Lesions ◽  
Oxygen Species ◽  
Dna Breaks ◽  
Site Specific

AbstractDNA repair requires reorganization of the local chromatin structure to facilitate access to and repair of the DNA. Studying DNA double-strand break (DSB) repair in specific chromatin domains has been aided by the use of sequence-specific endonucleases to generate targeted breaks. Here, we describe a new approach that combines KillerRed, a photosensitizer that generates reactive oxygen species (ROS) when exposed to light, and the genome-targeting properties of the CRISPR/Cas9 system. Fusing KillerRed to catalytically inactive Cas9 (dCas9) generates dCas9-KR, which can then be targeted to any desired genomic region with an appropriate guide RNA. Activation of dCas9-KR with green light generates a local increase in reactive oxygen species, resulting in “clustered” oxidative damage, including both DNA breaks and base damage. Activation of dCas9-KR rapidly (within minutes) increases both γH2AX and recruitment of the KU70/80 complex. Importantly, this damage is repaired within 10 minutes of termination of light exposure, indicating that the DNA damage generated by dCas9-KR is both rapid and transient. Further, repair is carried out exclusively through NHEJ, with no detectable contribution from HR-based mechanisms. Surprisingly, sequencing of repaired DNA damage regions did not reveal any increase in either mutations or INDELs in the targeted region, implying that NHEJ has high fidelity under the conditions of low level, limited damage. The dCas9-KR approach for creating targeted damage has significant advantages over the use of endonucleases, since the duration and intensity of DNA damage can be controlled in “real time” by controlling light exposure. In addition, unlike endonucleases that carry out multiple cut-repair cycles, dCas9-KR produces a single burst of damage, more closely resembling the type of damage experienced during acute exposure to reactive oxygen species or environmental toxins. dCas9-KR is a promising system to induce DNA damage and measure site-specific repair kinetics at clustered DNA lesions.

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