ArticleMolecular biology reports2026
Mechanistic role of Nrf2-Keap1 and JNK/p38 MAPK signaling in mercury-induced oxidative stress and apoptosis in monocytes/macrophages of Channa punctatus Bloch.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMercury (Hg) is a hazardous environmental contaminant that presents significant threats to aquatic life via oxidative stress-induced cellular damage. This study examined mercury-induced oxidative stress and its influence on the regulation of antioxidant and apoptotic signaling pathways in the monocytes/macrophages of Channa punctatus Bloch.
methodsAcclimatized fish were split into control and treatment groups are exposed to HgCl₂ (0.3 mg/L) for 7 days. Monocytes/macrophages were extracted and evaluated for ultrastructural modifications, oxidative stress indicators, antioxidant enzyme activity, and DNA damage. Reactive oxygen species (ROS), respiratory burst activity, lipid peroxidation, superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) concentrations were quantified. The expression of antioxidant signaling molecules (Nrf2, Keap1, and HO-1) was assessed, whereas apoptotic responses were examined via flow cytometry for caspase-3, caspase-8, caspase-9, TNF-α, p38, and p53, in conjunction with variations in cytochrome c protein levels.
resultsMercury exposure resulted in considerable ultrastructural damage and increased reactive oxygen species (ROS) formation, respiratory burst activity, lipid peroxidation, DNA fragmentation, and superoxide dismutase (SOD) activity, alongside reduced catalase (CAT) and glutathione (GSH) levels. Dysregulation of the Nrf2–Keap1 signaling pathway and diminished HO-1 expression signify compromised antioxidant defense. The elevated expression of caspase-3, caspase-8, caspase-9, TNF-α, p38, and p53 confirmed the activation of apoptotic pathways. Alterations in cytochrome c and the activation of the JNK/p38 MAPK pathway further evidenced mitochondrial malfunction and the induction of apoptosis.
conclusionsMercury exposure causes oxidative stress-related immune cell damage in C. punctatus by inhibiting antioxidant signaling and facilitating apoptosis through intrinsic and extrinsic pathways, with the JNK/p38-MAPK pathway acting as a crucial mechanistic connection.
Indexed as
Identifiers
41944909What OpenQuestion holds
Registered trials
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 OpenQuestion graph.