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Related Experiment Video

Updated: May 27, 2026

Efficient Gene Knockdown in the Liver via Intrasplenic Injection of Adeno-Associated Virus Serotype 8 (AAV8)-Delivered Small Hairpin RNA

Efficient Gene Knockdown in the Liver via Intrasplenic Injection of Adeno-Associated Virus Serotype 8 (AAV8)-Delivered Small Hairpin RNA

Published on: November 1, 2024

Niacin requirements for genomic stability.

James B Kirkland¹

¹Department of Human Health & Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1. jkirklan@uoguelph.ca

Mutation Research

|December 6, 2011

Summary

Niacin (vitamin B3) status impacts metabolism and genomic stability. Adequate niacin intake minimizes DNA damage and cancer risk, with potential benefits from higher doses, especially under stress.

Area of Science:

Biochemistry
Nutritional Science
Genetics

Background:

Niacin (vitamin B3) is essential for over 400 metabolic reactions.
Niacin deficiency is linked to genomic instability via impaired poly ADP-ribose polymerase (PARP) function.
Deficiency can lead to DNA damage, cell cycle issues, apoptosis, and cancer.

Purpose of the Study:

To review the role of niacin status in maintaining genomic stability.
To evaluate the impact of niacin intake levels on DNA repair and cancer development.
To assess the potential benefits of niacin supplementation in various populations and conditions.

Main Methods:

Review of existing literature on niacin, metabolism, and genomic instability.
Analysis of data from rat and mouse models regarding niacin intake and DNA damage.

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Last Updated: May 27, 2026

Efficient Gene Knockdown in the Liver via Intrasplenic Injection of Adeno-Associated Virus Serotype 8 (AAV8)-Delivered Small Hairpin RNA

Efficient Gene Knockdown in the Liver via Intrasplenic Injection of Adeno-Associated Virus Serotype 8 (AAV8)-Delivered Small Hairpin RNA

Published on: November 1, 2024

Consideration of human data and population studies on niacin status and health outcomes.

Main Results:

Niacin deficiency impairs DNA repair, cell cycle control, and promotes genomic instability.
Recommended niacin levels (AIN-93) in rat models minimize most genomic instability aspects.
Pharmacological niacin intakes show protection against UV-induced skin cancer in mouse models.

Conclusions:

Optimal niacin intake is crucial for preventing genomic instability and associated diseases.
Some human populations may have suboptimal niacin intake, benefiting from supplementation.
Higher niacin doses may offer protective benefits against DNA damage from stressors like chemotherapy or UV radiation.