Oxidative stress-related infantile pyknocytosis with Heinz bodies

Charlotte Stephan; Aurélie Phulpin; Dominique Steschenko; Jean-François Lesesve; Julien Perrin

doi:10.1111/trf.14467

Ribonuclease Inhibitor Protein of Human Erythrocytes: Characterization, Loss of Activity in Response to Oxidative Stress, and Association with Heinz Bodies

Blood Cells Molecules and Diseases ◽

10.1006/bcmd.1998.0182 ◽

1998 ◽

Vol 24 (2) ◽

pp. 149-164 ◽

Cited By ~ 18

Author(s):

Michel Moenner ◽

Mehrdad Vosoghi ◽

Sergey Ryazantsev ◽

Dohn G. Glitz

Keyword(s):

Oxidative Stress ◽

Human Erythrocytes ◽

Inhibitor Protein ◽

Ribonuclease Inhibitor ◽

Heinz Bodies

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The effects of superoxide dismutase knockout on the oxidative stress parameters and survival of mouse erythrocyt

Cellular & Molecular Biology Letters ◽

10.2478/s11658-008-0031-8 ◽

2009 ◽

Vol 14 (1) ◽

Cited By ~ 12

Author(s):

Agnieszka Grzelak ◽

Marcin Kruszewski ◽

Ewa Macierzyńska ◽

Łukasz Piotrowski ◽

Łukasz Pułaski ◽

...

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Blood Plasma ◽

Reticulocyte Count ◽

Thiobarbituric Acid ◽

Protective Effects ◽

Thiobarbituric Acid Reactive Substances ◽

Heinz Bodies ◽

Plasma Glutathione ◽

Activity Decrease

AbstractThe erythrocytes of 12-month old Sod1 −/− mice showed an increased level of reactive oxygen species (ROS), as estimated by the degree of dihydroethidine and dihydrorhodamine oxidation, and the increased level of Heinz bodies. No indices of severe oxidative stress were found in the red blood cells and blood plasma of Sod1 −/− mice as judged from the lack of significant changes in the levels of erythrocyte and plasma glutathione, plasma protein thiol and carbonyl groups and thiobarbituric-acid reactive substances in the blood plasma. However, a decreased erythrocyte lifespan, increased reticulocyte count and splenomegaly were noted, indicating the importance of superoxide dismutase for maintaining erythrocyte viability. The levels of erythrocyte ROS and Heinz bodies and the reticulocyte count were indistinguishable in Sod1 +/+ and Sod1 +/− mice, suggesting that a superoxide dismutase activity decrease to half of its normal value may be sufficient to secure the protective effects of the enzyme.

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Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp (Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

Food & Function ◽

10.1039/d0fo01638a ◽

2020 ◽

Vol 11 (10) ◽

pp. 8547-8559

Author(s):

Hongjing Zhao ◽

Yu Wang ◽

Mengyao Mu ◽

Menghao Guo ◽

Hongxian Yu ◽

...

Keyword(s):

Oxidative Stress ◽

Secondary Metabolites ◽

Human Health ◽

Grass Carp ◽

Aquatic Environment ◽

Ctenopharyngodon Idellus

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.

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Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

Biochemical Journal ◽

10.1042/bcj20190591 ◽

2019 ◽

Vol 476 (24) ◽

pp. 3705-3719 ◽

Cited By ~ 2

Author(s):

Avani Vyas ◽

Umamaheswar Duvvuri ◽

Kirill Kiselyov

Keyword(s):

Oxidative Stress ◽

Head And Neck ◽

Transcriptional Activation ◽

Platinum Resistance ◽

Mrna Levels ◽

Strong Positive Correlation ◽

Platinum Compounds ◽

Copper Chelation ◽

Novel Approach ◽

Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

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Clinical aspects of reactive oxygen and nitrogen species

Biochemical Society Symposium ◽

10.1042/bss0710121 ◽

2004 ◽

Vol 71 ◽

pp. 121-133 ◽

Cited By ~ 25

Author(s):

Ascan Warnholtz ◽

Maria Wendt ◽

Michael August ◽

Thomas Münzel

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Risk Factor ◽

Endothelial Dysfunction ◽

Vascular Tissue ◽

Rapid Development ◽

Reactive Oxygen ◽

Clinical Aspects ◽

No Production ◽

Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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