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Updated: Dec 13, 2025
Cell-Specific Paired Interrogation of the Mouse Ovarian Epigenome and Transcriptome
Published on: February 24, 2023
N1-Methylnicotinamide: An Anti-Ovarian Aging Hormetin?
Hamid Reza Nejabati1, Kathrin Schmeisser2, Vahideh Shahnazi3
1Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract:
Ovarian aging occurs due to the reduction of the quality and quantity of the oocytes, and is regulated by mitochondrial survival and apoptotic signals. Reactive Oxygen Species (ROS) are one of those signals considered detrimental to cellular homeostasis. Nowadays, ROS are regarded as a regulatory factor at low levels as it induces the stress resistance which in turn increases the longevity. It is believed that the main mechanism for the life-promoting role of the ROS mediated by the 5' Adenosine Monophosphate-activated Protein Kinase (AMPK). N1-Methylnicotinamide (MNAM) is well known for its anti-diabetic, anti-thrombotic, and anti-inflammatory activity. Aldehyde oxidase 1 (AOX1) is a detoxifying enzyme, which metabolizes the MNAM and produces two metabolites including N1-methyl-2-pyridone-5- carboxamide (2py) and N1-methyl-4-pyridone-3-carboxamide (4py). The activity of AOX1 enhances the production of ROS and improves the longevity. It has been reported that the MNAM could postpone the aging through the induction of low-level stress. It has been documented that the production of MNAM is significantly higher in the cumulus cells of the patients with Polycystic Ovary Syndrome (PCOS) and its administration on the rat model of PCOS has been shown to alleviate the hyperandrogenism and successfully activate the ovarian AMPK. Therefore, it can be hypothesized that the anti-ovarian aging effects of the MNAM are possibly based on the activation of AMPK through transient elevation of the ROS.
Insights
N1-Methylnicotinamide (MNAM) may combat ovarian aging by activating AMPK through increased Reactive Oxygen Species (ROS). This mechanism, involving Aldehyde Oxidase 1 (AOX1), shows potential for improving ovarian health and longevity.
Area of Science:
- Reproductive Biology
- Cellular Aging
- Biochemistry
Background:
- Ovarian aging is linked to decreased oocyte quality and quantity, influenced by mitochondrial and apoptotic signaling.
- Reactive Oxygen Species (ROS), often seen as detrimental, can promote stress resistance and longevity at low levels.
- 5' Adenosine Monophosphate-activated Protein Kinase (AMPK) is a key mediator of ROS's life-promoting effects.
Purpose of the Study:
- To investigate the potential anti-aging effects of N1-Methylnicotinamide (MNAM) on ovarian function.
- To explore the role of Reactive Oxygen Species (ROS) and AMPK activation in MNAM's proposed anti-aging mechanism.
- To understand the link between MNAM metabolism, ROS production, and ovarian longevity.
Main Methods:
- Examined the role of Aldehyde Oxidase 1 (AOX1) in metabolizing MNAM into 2py and 4py.
- Investigated how AOX1 activity influences ROS production and cellular longevity.
- Reviewed existing literature on MNAM, PCOS, and AMPK activation in ovarian aging models.
Main Results:
- AOX1 metabolizes MNAM, enhancing ROS production and potentially improving longevity.
- MNAM has demonstrated anti-aging properties by inducing low-level stress.
- Elevated MNAM levels are observed in Polycystic Ovary Syndrome (PCOS) patients, and MNAM administration improved PCOS rat models by activating ovarian AMPK.
Conclusions:
- MNAM's anti-ovarian aging effects are hypothesized to stem from AMPK activation via transient ROS elevation.
- The interplay between MNAM, AOX1, ROS, and AMPK presents a novel pathway for addressing ovarian aging.
- Further research into MNAM's therapeutic potential for age-related ovarian decline and PCOS is warranted.
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