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Molecules (Basel, Switzerland) Sep 2020Dental medicine is one of the fields of medicine where the most common pathologies are of bacterial and fungal origins. This review is mainly focused on the... (Review)
Review
Dental medicine is one of the fields of medicine where the most common pathologies are of bacterial and fungal origins. This review is mainly focused on the antimicrobial effects of cinnamon essential oil (EO), cinnamon extracts, and pure compounds against different oral pathogens and the oral biofilm and the possible effects on soft mouth tissue. Basic information is provided about cinnamon, as is a review of its antimicrobial properties against the most common microorganisms causing dental caries, endodontic and periodontal lesions, and candidiasis. Cinnamon EO, cinnamon extracts, and pure compounds show significant antimicrobial activities against oral pathogens and could be beneficial in caries and periodontal disease prevention, endodontics, and candidiasis treatment.
Topics: Acrolein; Acyclic Monoterpenes; Anti-Bacterial Agents; Anti-Infective Agents; Bacteria; Biofilms; Candida; Cinnamomum zeylanicum; Clinical Trials as Topic; Dental Caries; Eugenol; Humans; Microbial Sensitivity Tests; Oils, Volatile; Plant Bark; Plant Leaves; Polycyclic Sesquiterpenes
PubMed: 32932678
DOI: 10.3390/molecules25184184 -
Microbial Pathogenesis Jul 2018In the current healthcare environment, an alarming rise in multi-drug resistant bacterial infections has led to a global health threat. The lack of new antibiotics has... (Review)
Review
BACKGROUND
In the current healthcare environment, an alarming rise in multi-drug resistant bacterial infections has led to a global health threat. The lack of new antibiotics has created a need for developing alternative strategies.
OBJECTIVE
Understanding the antibacterial mechanisms of cinnamon and its constituents is crucial to enhance it as a potential new source of antibiotic. The objective of this review is to provide a compilation of all described mechanisms of antibacterial action of cinnamon and its constituents and synergism with commercial antibiotics in order to better understand how cinnamon and its constituents can collaborate as alternative treatment to multi-drug resistant bacterial infections.
METHODS
The relevant references on antibacterial activities of cinnamon and its constituents were searched. Meanwhile, the references were classified according to the type of mechanism of action against bacteria. Relationships of cinnamon or its constituents and antibiotics were also analyzed and summarized.
RESULTS
Cinnamon extracts, essential oils, and their compounds have been reported to inhibit bacteria by damaging cell membrane; altering the lipid profile; inhibiting ATPases, cell division, membrane porins, motility, and biofilm formation; and via anti-quorum sensing effects.
CONCLUSION
This review describes the antibacterial effects of cinnamon and its constituents, such as cinnamaldehyde and cinnamic acid, against pathogenic Gram-positive and Gram-negative bacteria. The review also provides an overview of the current knowledge of the primary modes of action of these compounds as well as the synergistic interactions between cinnamon or its constituents with known antibacterial agents. This information will be useful in improving the effectiveness of therapeutics based on these compounds.
Topics: Acrolein; Adenosine Triphosphatases; Anti-Bacterial Agents; Bacteria; Biofilms; Cell Division; Cell Membrane; Cinnamates; Cinnamomum zeylanicum; Databases, Factual; Drug Combinations; Drug Resistance, Multiple, Bacterial; Drug Synergism; Oils, Volatile; Plant Extracts; Porins; Quorum Sensing
PubMed: 29702210
DOI: 10.1016/j.micpath.2018.04.036 -
Aging Cell Apr 2022Acrolein, an unsaturated aldehyde, is increased in the brain of Alzheimer's disease (AD) patients and identified as a potential inducer of sporadic AD. Synaptic...
Acrolein, an unsaturated aldehyde, is increased in the brain of Alzheimer's disease (AD) patients and identified as a potential inducer of sporadic AD. Synaptic dysfunction, as a typical pathological change occurring in the early stage of AD, is most closely associated with the severity of dementia. However, there remains a lack of clarity on the mechanisms of acrolein inducing AD-like pathology and synaptic impairment. In this study, acrolein-treated primary cultured neurons and mice were applied to investigate the effects of acrolein on cognitive impairment and synaptic dysfunction and their signaling mechanisms. In vitro, ROCK inhibitors, Fasudil, and Y27632, could attenuate the axon ruptures and synaptic impairment caused by acrolein. Meanwhile, RNA-seq distinct differentially expressed genes in acrolein models and initially linked activated RhoA/Rho-kinase2 (ROCK2) to acrolein-induced synaptic dysfunction, which could regulate neuronal cytoskeleton and neurite. The Morris water maze test and in vivo field excitatory postsynaptic potential (fEPSP) were performed to evaluate spatial memory and long-term potential (LTP), respectively. Acrolein induced cognitive impairment and attenuated LTP. Furthermore, the protein level of Synapsin 1 and postsynaptic density 95 (PSD95) and dendritic spines density were also decreased in acrolein-exposed mice. These changes were improved by ROCK2 inhibitor Fasudil or in ROCK2 mice. Together, our findings suggest that RhoA/ROCK2 signaling pathway plays a critical role in acrolein-induced synaptic damage and cognitive dysfunction, suggesting inhibition of ROCK2 should benefit to the early AD.
Topics: Acrolein; Aldehydes; Alzheimer Disease; Animals; Disease Models, Animal; Hippocampus; Humans; Mice; rho-Associated Kinases; rhoA GTP-Binding Protein
PubMed: 35315217
DOI: 10.1111/acel.13587 -
Molecules (Basel, Switzerland) Nov 2023Polyamines participate in the processes of cell growth and development. The degradation branch of their metabolism involves amine oxidases. The oxidation of spermine,... (Review)
Review
Polyamines participate in the processes of cell growth and development. The degradation branch of their metabolism involves amine oxidases. The oxidation of spermine, spermidine and putrescine releases hydrogen peroxide and the corresponding aminoaldehyde. Polyamine-derived aminoaldehydes have been found to be cytotoxic, and they represent the subject of this review. 3-aminopropanal disrupts the lysosomal membrane and triggers apoptosis or necrosis in the damaged cells. It is implicated in the pathogenesis of cerebral ischemia. Furthermore, 3-aminopropanal yields acrolein through the elimination of ammonia. This reactive aldehyde is also generated by the decomposition of aminoaldehydes produced in the reaction of serum amine oxidase with spermidine or spermine. In addition, acrolein is a common environmental pollutant. It causes covalent modifications of proteins, including carbonylation, the production of Michael-type adducts and cross-linking, and it has been associated with inflammation-related diseases. APAL and acrolein are detoxified by aldehyde dehydrogenases and other mechanisms. High-performance liquid chromatography, immunochemistry and mass spectrometry have been largely used to analyze the presence of polyamine-derived aminoaldehydes and protein modifications elicited by their effect. However, the main and still open challenge is to find clues for discovering clear linkages between aldehyde-induced modifications of specific proteins and the development of various diseases.
Topics: Polyamines; Acrolein; Spermidine; Spermine; Aldehydes
PubMed: 37959847
DOI: 10.3390/molecules28217429 -
Scientific Reports May 2022Building-related symptoms (BRS) is a significant work-related and public health problem, characterized by non-specific symptoms occurring in a particular building. The...
Building-related symptoms (BRS) is a significant work-related and public health problem, characterized by non-specific symptoms occurring in a particular building. The cause of BRS is unknown, but certain reactive compounds are suggested risk factors. The aim of this controlled exposure study was to investigate whether BRS cases report more odor annoyance and symptoms and show altered autonomous nervous system (ANS) response during exposure to the reactive aldehyde, acrolein in comparison with referents. Individuals with BRS (n = 18) and referents (n = 14) took part in two exposure sessions (80 min). One session contained heptane alone, and the other heptane and acrolein. Perceived odor annoyance; eye, nose, and throat symptoms; and ANS response were measured continuously. BRS cases did not experience more odor annoyance; eye, nose, and throat symptoms; or altered ANS response in comparison with referents during the exposures. Supplementary analyses revealed that BRS cases that also reported chemical intolerance perceived more symptoms than referents during acrolein exposure. Acrolein exposure at a concentration below previously reported sensory irritation detection thresholds is perceived as more irritating by a subgroup of BRS individuals compared with referents. The results of this study indicate that a subset of individuals with building related symptoms (BRS) has a lowered sensory irritation threshold towards acrolein exposure. Future guidelines on chemical exposures to acrolein should take time and individual sensitivity into account.
Topics: Acrolein; Aldehydes; Heptanes; Humans; Odorants; Sensory Thresholds
PubMed: 35581334
DOI: 10.1038/s41598-022-12370-7 -
Molecular Nutrition & Food Research Sep 2011Acrolein, an α,β-unsaturated aldehyde, is a ubiquitous pollutant that is also produced endogenously through lipid peroxidation. This compound is hundreds of times more... (Review)
Review
Acrolein, an α,β-unsaturated aldehyde, is a ubiquitous pollutant that is also produced endogenously through lipid peroxidation. This compound is hundreds of times more reactive than other aldehydes such as 4-hydroxynonenal, is produced at much higher concentrations, and persists in solution for much longer than better known free radicals. It has been implicated in disease states known to involve chronic oxidative stress, particularly spinal cord injury and multiple sclerosis. Acrolein may overwhelm the anti-oxidative systems of any cell by depleting glutathione reserves, preventing glutathione regeneration, and inactivating protective enzymes. On the cellular level, acrolein exposure can cause membrane damage, mitochondrial dysfunction, and myelin disruption. Such pathologies can be exacerbated by increased concentrations or duration of exposure, and can occur in normal tissue incubated with injured spinal cord, showing that acrolein can act as a diffusive agent, spreading secondary injury. Several chemical species are capable of binding and inactivating acrolein. Hydralazine in particular can reduce acrolein concentrations and inhibit acrolein-mediated pathologies in vivo. Acrolein scavenging appears to be a novel effective treatment, which is primed for rapid translation to the clinic.
Topics: Acrolein; Animals; Central Nervous System; Humans; Mitochondria; Multiple Sclerosis; Myelin Sheath; Spinal Cord Injuries; Trauma, Nervous System
PubMed: 21823221
DOI: 10.1002/mnfr.201100217 -
Biomolecules Nov 2020Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical... (Review)
Review
Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical role in the pathogenesis of DR. Acrolein, a product of polyamines oxidation and lipid peroxidation, has been demonstrated to be involved in the pathogenesis of various human diseases. Acrolein's harmful effects are mediated through multiple mechanisms, including DNA damage, inflammation, ROS formation, protein adduction, membrane disruption, endoplasmic reticulum stress, and mitochondrial dysfunction. Recent investigations have reported the involvement of acrolein in the pathogenesis of DR. These studies have shown a detrimental effect of acrolein on the retinal neurovascular unit under diabetic conditions. The current review summarizes the existing literature on the sources of acrolein, the impact of acrolein in the generation of oxidative damage in the diabetic retina, and the mechanisms of acrolein action in the pathogenesis of DR. The possible therapeutic interventions such as the use of polyamine oxidase inhibitors, agents with antioxidant properties, and acrolein scavengers to reduce acrolein toxicity are also discussed.
Topics: Acrolein; Animals; Antioxidants; DNA Damage; Diabetic Retinopathy; Humans; Oxidative Stress; Retina
PubMed: 33233661
DOI: 10.3390/biom10111579 -
Frontiers in Immunology 2020With increasing prevalence of diabetes and a progressively aging society, diabetic retinopathy is emerging as one of the global leading causes of blindness. Recent... (Review)
Review
With increasing prevalence of diabetes and a progressively aging society, diabetic retinopathy is emerging as one of the global leading causes of blindness. Recent studies have shown that vascular endothelial growth factor (VEGF) plays a central role in the pathogenesis of diabetic retinopathy and anti-VEGF agents have become the first-line therapy for the vision-threatening disease. However, recent studies have also demonstrated that diabetic retinopathy is a multifactorial disease and that VEGF-independent mechanism(s) also underlie much of the pathological changes in diabetic retinopathy. Acrolein is a highly reactive unsaturated aldehyde and is implicated in protein dysfunction. As acrolein is common in air pollutants, previous studies have focused on it as an exogenous causative factor, for instance, in the development of respiratory diseases. However, it has been discovered that acrolein is also endogenously produced and induces cell toxicity and oxidative stress in the body. In addition, accumulating evidence suggests that acrolein and/or acrolein-conjugated proteins are associated with the molecular mechanisms in diabetic retinopathy. This review summarizes the pathological roles and mechanisms of endogenous acrolein production in the pathogenesis of diabetic retinopathy.
Topics: Acrolein; Animals; Diabetic Retinopathy; Humans
PubMed: 33193419
DOI: 10.3389/fimmu.2020.589531 -
Chemical Research in Toxicology Oct 2022Bacteria harboring glycerol/diol dehydratase (GDH) encoded by the genes CDE metabolize glycerol and release acrolein during growth. Acrolein has antimicrobial activity,...
Bacteria harboring glycerol/diol dehydratase (GDH) encoded by the genes CDE metabolize glycerol and release acrolein during growth. Acrolein has antimicrobial activity, and exposure of human cells to acrolein gives rise to toxic and mutagenic responses. These biological responses are related to acrolein's high reactivity as a chemical electrophile that can covalently bind to cellular nucleophiles including DNA and proteins. Various food microbes and gut commensals transform glycerol to acrolein, but there is no direct evidence available for bacterial glycerol metabolism giving rise to DNA adducts. Moreover, it is unknown whether pathogens, such as Typhymurium, catalyze this transformation. We assessed, therefore, acrolein formation by four GDH-competent strains of Typhymurium grown under either aerobic or anaerobic conditions in the presence of 50 mM glycerol. On the basis of analytical derivatization with a heterocyclic amine, all wild-type strains were observed to produce acrolein, but to different extents, and acrolein production was not detected in fermentations of a C-deficient mutant strain. Furthermore, we found that, in the presence of calf thymus DNA, acrolein-DNA adducts were formed as a result of bacterial glycerol metabolism by two strains of , but not a CDE mutant strain. The quantification of the resulting adducts with increasing levels of glycerol up to 600 mM led to the production of up to 1.5 mM acrolein and 3600 acrolein-DNA adducts per 10 nucleosides in a model system. These results suggest that GDH-competent food microbes, gut commensals, and pathogens alike have the capacity to produce acrolein from glycerol. Further, the acrolein production can lead to DNA adduct formation, but requires high glycerol concentrations that are not available in the human gut.
Topics: Acrolein; Amines; Anti-Infective Agents; Bacteria; DNA; DNA Adducts; Glycerol; Humans; Propanediol Dehydratase
PubMed: 36116084
DOI: 10.1021/acs.chemrestox.2c00137 -
Molecular Nutrition & Food Research Jan 2008Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids... (Review)
Review
Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids during heating of foods, and by combustion of petroleum fuels and biodiesel. Chemical reactions responsible for release of acrolein include heat-induced dehydration of glycerol, retro-aldol cleavage of dehydrated carbohydrates, lipid peroxidation of polyunsaturated fatty acids, and Strecker degradation of methionine and threonine. Smoking of tobacco products equals or exceeds the total human exposure to acrolein from all other sources. The main endogenous sources of acrolein are myeloperoxidase-mediated degradation of threonine and amine oxidase-mediated degradation of spermine and spermidine, which may constitute a significant source of acrolein in situations of oxidative stress and inflammation. Acrolein is metabolized by conjugation with glutathione and excreted in the urine as mercapturic acid metabolites. Acrolein forms Michael adducts with ascorbic acid in vitro, but the biological relevance of this reaction is not clear. The biological effects of acrolein are a consequence of its reactivity towards biological nucleophiles such as guanine in DNA and cysteine, lysine, histidine, and arginine residues in critical regions of nuclear factors, proteases, and other proteins. Acrolein adduction disrupts the function of these biomacromolecules which may result in mutations, altered gene transcription, and modulation of apoptosis.
Topics: Acrolein; Amino Acids; Ascorbic Acid; Carbohydrates; Cell Death; DNA Adducts; Environmental Exposure; Fatty Acids, Unsaturated; Food; Glutathione; Hot Temperature; Humans; Lipids; Oxidative Stress; Threonine; Nicotiana
PubMed: 18203133
DOI: 10.1002/mnfr.200700412