Evidence map›Paper›PMID 39623245›Full record

ArticlePharmacological reports : PR2025

Proteomics analysis in rats reveals convergent mechanisms between major depressive disorder and dietary zinc deficiency.

Łukasz Gąsior, Bartłomiej Pochwat, Monika Zaręba-Kozioł, Jakub Włodarczyk, Andreas Martin Grabrucker, Bernadeta Szewczyk

Abstract read
In one paragraph

Article in Pharmacological reports : PR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Bioinformatics Analysis of the Diagnostic Value of Copper and Zinc Metabolism-Related Genes in Major Depressive Disorder: An In Silico Multi-Cohort Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Łukasz GąsiorMaj Institute of Pharmacology, Department of Neurobiology, Polish Academy of Sciences, Smętna 12, Kraków, 31-343, Poland. gasior@if-pan.krakow.pl.
Bartłomiej PochwatMaj Institute of Pharmacology, Department of Neurobiology, Polish Academy of Sciences, Smętna 12, Kraków, 31-343, Poland.
Monika Zaręba-KoziołLaboratory of Cell Biophysics, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Ludwika Pasteura 3, Warsaw, 02-093, Poland.
Jakub WłodarczykLaboratory of Cell Biophysics, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Ludwika Pasteura 3, Warsaw, 02-093, Poland.
Andreas Martin GrabruckerDept. of Biological Sciences, University of Limerick, Limerick, V94PH61, Ireland.
Bernadeta SzewczykMaj Institute of Pharmacology, Department of Neurobiology, Polish Academy of Sciences, Smętna 12, Kraków, 31-343, Poland. szewczyk@if-pan.krakow.pl.

Funding

Narodowym Centrum Nauki UMO- 2019/35/D/NZ4/02042
6 · The paper itself

Abstract

backgroundPreclinical and clinical studies have shown that dietary zinc deficiency can lead to symptoms similar to those observed in major depressive disorder (MDD). However, the underlying molecular mechanisms remain unclear. To investigate these mechanisms, we examined proteomic changes in the prefrontal cortex (PFC) and hippocampus (HP) of rats, two critical brain regions implicated in the pathophysiology of depression.

methodsRats were fed diets either adequate in zinc (ZnA, 50 mg Zn/kg) or deficient in zinc (ZnD, <3 mg/kg) for four weeks. High-throughput proteomic analysis was used to detect changes in protein expression, supplemented by enzyme activity assay for mitochondrial complexes I and IV, examining their functional impacts.

resultsZnD led to significant alterations in protein expression related to zinc transport and mitochondrial function. Proteomic analysis revealed changes in zinc transporter family members such as Slc30a1 (6.64 log2FC), Slc30a3 (-2.32 log2FC), Slc30a4 (2.87 log2FC), Slc30a5 (5.90 log2FC), Slc30a6 (1.50 log2FC), and Slc30a7 (2.17 log2FC) in the PFC, and Slc30a3 (-1.02 log2FC), Slc30a5 (-1.04 log2FC), and Slc30a7 (1.08 log2FC) in the HP of rats subjected to ZnD. Furthermore, ZnD significantly affected essential mitochondrial activity proteins, including Atp5pb (3.25 log2FC), Cox2 (2.28 log2FC), Atp5me (2.04 log2FC), Cyc1 (2.30 log2FC), Cox4i1 (1.23 log2FC), Cox7c (1.63 log2FC), and Cisd1 (1.55 log2FC), with a pronounced decrease in complex I activity in the PFC.

conclusionsOur study demonstrates that ZnD leads to significant proteomic changes in the PFC and HP of rats. Specifically, ZnD alters the expression of zinc transporter proteins and proteins critical for mitochondrial function. The significant decrease in complex I activity in the PFC further underscores the impact of ZnD on mitochondrial function. These results highlight the molecular mechanisms by which ZnD can influence brain function and contribute to symptoms similar to those observed in depression.

Indexed as

Major Depressive DisorderZincAnimalsDietDisease Models, AnimalHippocampusMaleMitochondriaPrefrontal CortexProteomicsRatsRats, Sprague-DawleyZincDepressionMitochondrial dysfunctionProteomic analysisZinc deficiency

Identifiers

PMID39623245
PMCPMC11743416

What Socratic holds

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Registered trials

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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.