Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Sulfur Assimilation

Sulfur Assimilation

Sulfur is an essential element in biological systems, contributing to synthesizing key biomolecules, including amino acids such as cysteine and methionine, and cofactors such as coenzyme A and biotin. Microorganisms primarily assimilate sulfur as sulfate (SO₄²⁻) from the environment, which must undergo a series of biochemical transformations before it can be incorporated into cellular components. As sulfate is highly oxidized, it must undergo assimilatory sulfate reduction to become...

Role of Reduced Coenzymes NADH and FADH₂

Role of Reduced Coenzymes NADH and FADH₂

The energy released from the breakdown of the chemical bonds within nutrients can be stored either through the reduction of electron carriers or in the bonds of adenosine triphosphate (ATP). In living systems, a small class of compounds functions as mobile electron carriers, molecules that bind to and shuttle high-energy electrons between compounds in pathways. The principal electron carriers that will be considered originate from the B vitamin group and are derivatives of nucleotides; they are...

Redox Reactions

Redox Reactions

Redox reactions are vital biochemical processes that underpin energy metabolism in cells. These reactions involve the transfer of electrons between molecules, occurring in tandem as oxidation and reduction. Oxidation refers to the loss of electrons, while reduction denotes their gain. This coupling ensures the seamless flow of electrons through metabolic pathways. For example, in bacterial metabolism, glucose undergoes oxidation to carbon dioxide, while oxygen is simultaneously reduced to...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Blood DNA methylation and breast cancer risk: a prospective nested case-control study.

EBioMedicine·2026

Same author

How hyperoxia affects systemic redox state: insights from PULSE-Ox, a randomised double-blind mechanistic feasibility trial.

BJA open·2026

Same author

Frequency of MRI abnormalities in adult-onset MOG-IgG-associated disease at disease presentation: A cohort of Latin American patients.

Multiple sclerosis and related disorders·2026

Same author

Ciliary Zonule of the Human Eye: Structural and Mechanical Aspects.

Investigative ophthalmology & visual science·2026

Same author

Evidence based management of popliteal vessel injuries: A critical review, updates and controversies in the management of a difficult injury.

Injury·2026

Same author

Liposomal encapsulation of L-arginine and L-citrulline enhances pharmacokinetics and therapeutic effects in a model of preeclampsia and fetal growth restriction.

Scientific reports·2026

Search research articles

Related Experiment Video

Updated: May 25, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

Nitroso-redox status and vascular function in marginal and severe ascorbate deficiency.

Maria-Francisca Garcia-Saura¹, Fumito Saijo, Nathan S Bryan

¹Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts, USA.

Antioxidants & Redox Signaling

|February 7, 2012

Summary

Marginal vitamin C (ascorbic acid) deficiency impacts cardiovascular health by altering nitric oxide (NO) and redox balance. Studies show dynamic changes in NO/redox status and enhanced vascular reactivity during depletion.

More Related Videos

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Intradermal Microdialysis: An Approach to Investigating Novel Mechanisms of Microvascular Dysfunction in Humans

Intradermal Microdialysis: An Approach to Investigating Novel Mechanisms of Microvascular Dysfunction in Humans

Published on: July 21, 2023

Related Experiment Videos

Last Updated: May 25, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Intradermal Microdialysis: An Approach to Investigating Novel Mechanisms of Microvascular Dysfunction in Humans

Intradermal Microdialysis: An Approach to Investigating Novel Mechanisms of Microvascular Dysfunction in Humans

Published on: July 21, 2023

Area of Science:

Cardiovascular Science
Nutritional Biochemistry
Redox Biology

Background:

Marginal vitamin C (ascorbic acid) deficiency is an underappreciated cardiovascular disease risk factor.
Ascorbate and glutathione are crucial for antioxidant defense and redox signaling.
The interplay of nitric oxide (NO) and reactive oxygen species is key in redox regulation.

Purpose of the Study:

To investigate dynamic changes in NO/redox status and vascular function during ascorbate depletion in rats.
To understand the in vivo significance of ascorbate's role in redox signaling.

Main Methods:

Inducing ascorbate depletion in rats unable to synthesize vitamin C.
Monitoring time-course changes in NO/redox status in blood and organs.
Assessing vascular function, specifically aortic endothelial reactivity.

Main Results:

Ascorbate deficiency dynamically alters redox and protein nitros(yl)ation status in blood and tissues.
Marginal deficiency leads to cell/tissue-specific perturbations in ascorbate, glutathione, and NO status.
Enhanced NO production and protein nitros(yl)ation are responses to ascorbate deprivation, with paradoxically enhanced aortic endothelial reactivity.

Conclusions:

Enhanced NO production and nitros(yl)ation are integral responses to ascorbate deprivation-induced redox stress.
Cardiovascular risk in marginal deficiency may stem from NO/redox-sensitive signaling perturbations beyond vascular tone regulation.
This study provides a model for investigating redox-sensitive events in marginal ascorbate deficiency.