ArticleMolecules (Basel, Switzerland)2026
Genistein Protects Against Lead-Induced Cognitive Impairment Through a Glutathione-Dependent Redox-Mitochondrial Apoptosis Axis.
Article in Molecules (Basel, Switzerland), 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
5 authors.
Funding
Abstract
Lead exposure remains a pervasive environmental and public health threat, imposing a substantial burden of neurodevelopmental and cognitive dysfunction, yet safe mechanism-oriented interventions remain limited. Genistein, a soybean-derived isoflavone with antioxidant and neuroprotective potential, may counter heavy metal-induced neural injury; however, whether its efficacy is associated with redox-metabolic remodeling is unclear. Here, we evaluated genistein in lead-exposed C57BL/6J mice and lead-challenged HT22 hippocampal neurons. Genistein improved novel-arm exploration and spatial memory without altering locomotor or swimming performance, and attenuated neuronal disorganization and apoptosis in hippocampal CA1, CA3 and dentate gyrus regions. These protective effects were accompanied by reduced blood and hippocampal lead accumulation, restored glutathione redox balance, enhanced antioxidant capacity, preserved mitochondrial integrity, and suppressed Bax/Caspase-3-associated apoptotic signaling. Importantly, because genistein also reduced hippocampal lead accumulation, the in vivo neuroprotection may reflect both reduced target-tissue lead burden and improved glutathione-related redox homeostasis. Untargeted metabolomics identified 59 genistein-responsive metabolites enriched mainly in glutathione metabolism, oxidative phosphorylation, and ascorbate/aldarate metabolism, linking metabolic remodeling to behavioral recovery and reduced oxidative-apoptotic injury. In HT22 cells, blockade of glutathione synthesis by buthionine sulfoximine markedly weakened genistein-mediated cytoprotection, mitochondrial membrane potential recovery, and apoptosis inhibition. Collectively, genistein mitigates lead-induced hippocampal neurotoxicity and cognitive impairment by restoring glutathione-centered redox-mitochondrial homeostasis, supporting its further development as a mechanistically defined dietary candidate for environmental pollutant-associated neural injury.
Indexed as
Identifiers
What 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.