In vivo exposure to hydroquinone during the early phase of collagen-induced arthritis aggravates the disease

Heluany, Cíntia Scucuglia; Kupa, Léonard de Vinci Kanda; Viana, Mariana Nascimento; Fernandes, C.M.; Silveira, Eduardo Lani Volpe da; Farsky, Sandra Helena Poliselli

doi:10.1016/j.tox.2018.06.010

Cited by 11 publications

(8 citation statements)

References 49 publications

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“…A number of phytochemicals (including HQ) are shown to have antioxidative effects against oxidative stress (Andersen et al, 2010;Donnapee et al, 2014). But HQ, as a phytochemical, is shown to have pro-oxidant properties (Heluany et al, 2018). The 8-Isoprostane level is a well-known oxidative stress marker.…”

Section: Discussionmentioning

confidence: 99%

Antiplatelet, antioxidative, and anti‐inflammatory effects of hydroquinone

Chang

Pan

et al. 2019

Journal Cellular Physiology

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Platelets play crucial roles in thrombosis and hemostasis through platelet activation and aggregation that are crucial in cardiovascular diseases. Hydroquinone (HQ) and its derivatives are present in many dermatological creams, paints, motor fuels, air, microorganisms, and plant products like wheat bread, fruit, coffee, and red wine. The effect of HQ on humans is not clear. In this study, we found that HQ (>25 μM) inhibited arachidonic acid (AA)‐induced platelet aggregation. HQ suppressed AA‐induced thromboxane B2 production of platelets. HQ (>10 μM) also attenuated ex vivo platelet‐rich plasma aggregation. HQ prevented the interleukin (IL)‐1β‐induced 8‐isoprostane, and PGE2 production, but not IL‐8 production of pulp cells. These results indicate that HQ may have an antiplatelet effect via inhibition of thromboxane production. HQ has antioxidative and anti‐inflammatory effects, and possible inhibition of COX. Exposure and consumption of HQ‐containing products, food or drugs may have antiplatelet, antioxidative, and anti‐inflammatory effects.

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Section: Discussionmentioning

confidence: 99%

Antiplatelet, antioxidative, and anti‐inflammatory effects of hydroquinone

Chang

Pan

et al. 2019

Journal Cellular Physiology

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“…The modulation of the cytosolic transcription factor aryl hydrocarbon receptor (AhR) linked to BZ toxicity on BM and blood cells has recently been investigated. AhR is a ligand-activated transcription factor expressed in hematopoietic progenitor cells, lymphocytes, neutrophils, and splenocytes [ 132 , 133 , 134 ]. The connection between BZ exposure and AhR was first demonstrated by studies that provided evidence that hematopoietic toxicity induced by BZ was not observed in AhR knockout mice, but that toxicity would take place when the BM of animals was repopulated with cells from wild-type mice.…”

Section: Cellular and Molecular Mechanisms Of Toxicity On Hematopomentioning

confidence: 99%

“…Although HQ-exposed animals had no alterations in BM or blood cell numbers, disease symptoms worsened, with a high frequency of AhR + neutrophils and Th17 lymphocytes in the inflamed synovia. Accordingly, rheumatoid arthritis symptoms were not observed in AhR knockout mice exposed to HQ [ 133 , 134 ] (Heluany et al, under review). These data evidence that exposure to BZ metabolites worsens rheumatoid arthritis involving HQ actions through AhR on blood cells, and that both BZ and HQ are cigarette compounds involved with the harmful effects on the evolution of the disease as a result of cigarette smoking.…”

Section: Cellular and Molecular Mechanisms Of Toxicity On Hematopomentioning

confidence: 99%

Cellular and Molecular Mechanisms of Environmental Pollutants on Hematopoiesis

Scharf

Broering

Rocha

et al. 2020

IJMS

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Hematopoiesis is a complex and intricate process that aims to replenish blood components in a constant fashion. It is orchestrated mostly by hematopoietic progenitor cells (hematopoietic stem cells (HSCs)) that are capable of self-renewal and differentiation. These cells can originate other cell subtypes that are responsible for maintaining vital functions, mediate innate and adaptive immune responses, provide tissues with oxygen, and control coagulation. Hematopoiesis in adults takes place in the bone marrow, which is endowed with an extensive vasculature conferring an intense flow of cells. A myriad of cell subtypes can be found in the bone marrow at different levels of activation, being also under constant action of an extensive amount of diverse chemical mediators and enzymatic systems. Bone marrow platelets, mature erythrocytes and leukocytes are delivered into the bloodstream readily available to meet body demands. Leukocytes circulate and reach different tissues, returning or not returning to the bloodstream. Senescent leukocytes, specially granulocytes, return to the bone marrow to be phagocytized by macrophages, restarting granulopoiesis. The constant high production and delivery of cells into the bloodstream, alongside the fact that blood cells can also circulate between tissues, makes the hematopoietic system a prime target for toxic agents to act upon, making the understanding of the bone marrow microenvironment vital for both toxicological sciences and risk assessment. Environmental and occupational pollutants, therapeutic molecules, drugs of abuse, and even nutritional status can directly affect progenitor cells at their differentiation and maturation stages, altering behavior and function of blood compounds and resulting in impaired immune responses, anemias, leukemias, and blood coagulation disturbances. This review aims to describe the most recently investigated molecular and cellular toxicity mechanisms of current major environmental pollutants on hematopoiesis in the bone marrow.

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“…Hydroquinone has aggravated systemic and local ra symptoms in in vivo rodent models, due to the migration of aryl hydrocarbon receptors into synovia, higher serum levels of anti -citrullinated peptides and of proinflammatory cytokines. The large number of neutrophils in the synovial fluid activate aryl hydrocarbon receptors and the interleukin 17 pathway, which are involved in immune-mediated diseases (21,22).…”

Section: Quinonesmentioning

confidence: 99%

Etiopathogenic mechanisms of tobacco constituents in rheumatoid arthritis

Macovei¹,

Cardoneanu²,

Burlui³

et al. 2019

Ro J Rheumatol.

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Active smoking is considered a risk factor for rheumatoid arthritis. Smokers show respiratory extra-articular manifestations and complications, such as interstitial lung disease and chronic obstructive pulmonary disease. Smokers may receive a more intensive drug therapy than non-smokers, but they have a poor prognosis. Smoker's resistance to therapy may be caused by the pharmacokinetic interactions between drugs and tobacco constituents. The present account of some of those thousands of components of the gas and tar phase of cigarette smoke (polynuclear aromatic hydrocarbons, quinones, cyanide, heavy metals, bacterial endotoxins, nicotine and carbon monoxide) may help explain the inconclusive incrimination of tobacco use in the development of rheumatoid arthritis and convince more clinicians to recommend smoking cessation.

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In vivo exposure to hydroquinone during the early phase of collagen-induced arthritis aggravates the disease

Cited by 11 publications

References 49 publications

Antiplatelet, antioxidative, and anti‐inflammatory effects of hydroquinone

Antiplatelet, antioxidative, and anti‐inflammatory effects of hydroquinone

Cellular and Molecular Mechanisms of Environmental Pollutants on Hematopoiesis

Etiopathogenic mechanisms of tobacco constituents in rheumatoid arthritis

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