Evidence mapPaperPMID 41898526Full record

ArticleInternational journal of molecular sciences2026

Morphofunctional State of the Liver Under Conditions of Three-Month Dark Deprivation: The Influence of Circadian Disruptions and Melatonin.

David A Areshidze, Maria A Kozlova, Anna I Anurkina, Valeriy P Chernikov

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Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

4 authors.

David A AreshidzeAvtsyn Research Institute of Human Morphology of Petrovsky National Research Centre of Surgery, 117418 Moscow, Russia.ORCID 0000-0003-3006-6281
Maria A KozlovaAvtsyn Research Institute of Human Morphology of Petrovsky National Research Centre of Surgery, 117418 Moscow, Russia.
Anna I AnurkinaAvtsyn Research Institute of Human Morphology of Petrovsky National Research Centre of Surgery, 117418 Moscow, Russia.ORCID 0009-0003-0011-1114
Valeriy P ChernikovAvtsyn Research Institute of Human Morphology of Petrovsky National Research Centre of Surgery, 117418 Moscow, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of circadian rhythms caused by constant artificial lighting ("light pollution") is a significant risk factor for the development of metabolic and age-associated pathologies. The liver, as a central metabolic organ with pronounced circadian regulation of its functions, is particularly vulnerable to desynchronosis. The aim of this study was to evaluate the effect of three-month dark deprivation (constant lighting) and the corrective action of exogenous melatonin on the morphofunctional state of the liver in young mature rats. The experiment used 3-month-old male Wistar rats, divided into groups: control (standard light:dark cycle 10:14 h), dark deprivation group (DD, constant lighting 24 h/day), and DD + Melatonin group (DD + Mel, dark deprivation with melatonin administered in drinking water at a dose of 12 mg/L). After 3 months (animal age 6 months), a comprehensive analysis was performed. It was shown that dark deprivation causes a profound (more than five-fold) suppression of plasma melatonin levels, which is accompanied by the formation of a pro-senescent and metabolically dysfunctional phenotype of the liver. This was manifested by the development of steatosis, an 18% increase in hepatocyte area, a 30% decrease in the proportion of binucleated hepatocytes, activation of cellular senescence markers (p16, p21) and stress markers (p53), and suppression of the expression of circadian transcription factors BMAL1 and CLOCK. At the ultrastructural level, lipofuscin accumulation, damage to mitochondria and the Golgi apparatus were noted. Biochemically, hyperglycemia, increased AST activity, hypoproteinemia, hypoalbuminemia, hypercholesterolemia, and hypertriglyceridemia were revealed. Administration of exogenous melatonin completely prevented the development of these disorders, normalizing hormone levels, morphology, ultrastructure, biochemical parameters, and the expression of key molecular markers. Thus, three-month dark deprivation induces complex pro-senescent remodeling and metabolic dysfunction of the liver, mediated by melatonin deficiency, while exogenous melatonin demonstrates a pronounced hepatoprotective and chronoprotective effect.

Indexed as

Circadian RhythmLiverMelatoninAnimalsDarknessHepatocytesMaleRatsRats, WistarMelatoninagingcircadian rhythmsconstant lightingdark deprivationdesynchronosishepatocyteslivermelatoninsteatosis

Identifiers

PMID41898526
PMCPMC13027206

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.