What this means
Chronic circadian rhythm disruption, particularly constant light exposure (dark deprivation), is considered a factor that accelerates aging. However, the role of mitochondrial dysfunction in this process and the possibilities of its pharmacological correction remain insufficiently understood.
A plain-English summary is on its way. Until then, this is the start of the authors' own summary.
- Who it was tested in
- Animals or cells
- Kind of research
- Research in animals or cells
The science
- Original title
- [Quantitative electron microscopic assessment of the mitochondrial apparatus of hepatocytes during aging: Effect of constant illumination and melatonin correction.].
- Authors
- Аreshidze DA, Kozlova MA, Chernikov VP et al.
- Journal
- Advances in gerontology = Uspekhi gerontologii
- Published
- Oct 27, 2026
- Study type
- Lab or animal study · indexed as animal research
- PMID
- 42935343 ↗
Abstract
Chronic circadian rhythm disruption, particularly constant light exposure (dark deprivation), is considered a factor that accelerates aging. However, the role of mitochondrial dysfunction in this process and the possibilities of its pharmacological correction remain insufficiently understood. The aim of this study was to perform a quantitative ultrastructural assessment of the mitochondrial apparatus of rat hepatocytes during aging under constant light exposure and with exogenous melatonin supplementation. Male Wistar rats (n=480), starting from 3 months of age, were divided into three groups: control (10:14 h light/dark cycle), constant light group, and constant light group with melatonin added to drinking water (12 mg/L, 5 times/week). At 6, 12, 18, and 24 months of age, electron microscopic examination of the liver was performed with assessment of numerical density, area, perimeter, cristae count, form factor (circularity, C), and mitochondrial inner membrane coefficient (MIMC). Constant light exposure induced progressive accelerated mitochondrial aging: decreased numerical density, cristae number and length, organelle deformation, and massive hepatocyte death by 24 months. Melatonin administration prevented these alterations: the form factor was maintained at 0.80, while mitochondrial density and cristae count remained comparable to control. Chronic desynchronosis induces mitochondrial dysfunction as a key mechanism of accelerated liver aging. Exogenous melatonin exerts a potent mitochondria-protective effect, stabilizing the ultrastructure and energy apparatus of hepatocytes, which substantiates its further investigation as a geroprotector in circadian disorders.
Аreshidze DA, Kozlova MA, Chernikov VP et al. [Quantitative electron microscopic assessment of the mitochondrial apparatus of hepatocytes during aging: Effect of constant illumination and melatonin correction.]. Advances in gerontology = Uspekhi gerontologii. 2026. doi:10.34922/AE.2026.39.4.017. PMID: 42935343. https://pubmed.ncbi.nlm.nih.gov/42935343/