Skip to content
DraconiticResearch
Search Sources API
190,851 studies31 sourcesUpdated 28 min ago
Peer-reviewedCC BY 4.0BioTechnologia

Prosopis africana protects against heavy metal mixture-induced pulmonary and hematological toxicity via nuclear factor erythroid 2-related factor 2/ nuclear factor-kappa B/ caspase-3 signaling

4 affiliations
  1. 1African Centre of Excellence for Public Health and Toxicological Research, University of Port Harcourt, Choba, Nigeria
  2. 2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Enugu State University of Science and Technology, Enugu, Nigeria
  3. 3Department of Experimental Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, University of Port Harcourt, Port Harcourt, Nigeria
  4. 4Advanced Research Centre, European University of Lefke, Lefke, Northern Cyprus

Abstract

Background: Heavy metal mixture (HMM) exposure poses severe health risks by inducing oxidative stress and inflammation. The limitations of conventional chelation therapy necessitate exploring natural alternatives. Although Prosopis africana (PA) has antioxidant properties, its potential as a protective agent remains underexplored. This study investigated the protective mechanisms of PA against lead/ cadmium/arsenic-induced pulmonary and hematological toxicity.

Materials and methods: Rats were treated with HMM alone or combined with PA (500, 1000, or 1500 mg/kg). The evaluated parameters included lung and blood metal accumulation, oxidative stress markers (malondialdehyde, nitric oxide), antioxidant defenses (superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase), inflammatory cytokines (interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α]), transcription factors (nuclear factor erythroid 2-related factor 2 [Nrf2], nuclear factor kappa B [NF-κB]), caspase-3, hematological parameters, and lung histopathology. Multivariate analyses were applied to integrate biomarker patterns.

Results: HMM exposure significantly increased tissue metal levels, oxidative stress, inflammatory mediators, and caspase-3 activity, while suppressing antioxidant defenses and disrupting hematological parameters and lung architecture. PA co-treatment reversed these changes in a dose-dependent manner. At 1500 mg/kg, PA reduced blood metal levels by > 90%, normalized the oxidative-antioxidant balance, decreased IL-6 and TNF-α by 60–70%, suppressed caspase-3 activity by 90%, restored hematological indices, and ameliorated lung damage. Principal component and hierarchical cluster analyses clearly separated the HMM-exposed groups from the PA-treated groups based on their distinct oxidative, inflammatory, and protective profiles.

Conclusions: PA protects against HMM-induced toxicity by reducing metal bioavailability – potentially via chelation and/or altered absorption or excretion – coupled with Nrf2 activation and NF-κB/caspase-3 suppression. These findings suggest its potential as an adjunct therapy for heavy metalinduced pathologies.

Related

  1. QUERCETIN DISRUPTS NUCLEAR FACTOR ERYTHROID 2–RELATED FACTOR 2 SURVIVAL SIGNALING AND ACTIVATES A PRO-APOPTOTIC MICRORNA PROGRAM IN ACUTE MYELOID LEUKEMIA
    Marisa Claudia ALVAREZ, Karla Priscila FERRO, Irene Marisa SANTOS +4
    Hematology, Transfusion and Cell TherapyPeer-reviewedCC BYFull textEndocrinology & metabolismDOAJ
  2. β‐sitosterol Alleviates Pulmonary Arterial Hypertension in Rats With Involvement of the VEGF/PI3K/AKT Signaling Pathway
    Xiaobing Wu, Chen Gong, Zhiyu Zeng
    Pulmonary circulationPeer-reviewedCC BY-NCFull textGeneral medicineEurope PMC
  3. High-Calorie Diet Aggravates Lipopolysaccharide-Induced Pulmonary Inflammation in Juvenile Mice: Association of Acetate-Mediated Macrophage Polarization with AMPK/YAP Signaling
    Futongyu Sun, Hui Liu, Shuxuan Li +6
    NutrientsPeer-reviewedCC BYFull textNutritionEurope PMC
  4. Effect of Activin Type II Receptor Signaling in Patients With HFpEF and Pulmonary Hypertension: A Critical Analysis of Biological Mechanisms and Clinical Trials
    Milton Packer, Mardi Gomberg-Maitland, Ryan J. Tedford +3
    CirculationPeer-reviewedCC BYFull textCardiovascular medicineEurope PMC
  5. Inhibiting MD2 activates AMPK-dependent PPARγ/NOX4 signaling to attenuate mitochondrial oxidative stress and relieve pulmonary hypertension
    Jun Chen, Mengyu Chai, Yichen Liu +10
    Redox BiologyPeer-reviewedCC BY-NC-ND 4.0Full textMolecular biology & gene regulationGeneral biologyDOAJPMC
BibTeX
@article{ozoani2026prosopis,
  title = {{Prosopis africana protects against heavy metal mixture-induced pulmonary and hematological toxicity via nuclear factor erythroid 2-related factor 2/ nuclear factor-kappa B/ caspase-3 signaling}},
  author = {Harrison A. Ozoani and Kenneth O. Okolo and Baridoo Donatus Dooka and Cecilia N. Obasi and Prosper Manu Abdulai and Orish E. Orisakwe},
  journal = {BioTechnologia},
  year = {2026},
  month = sep,
  doi = {10.5114/bta/223960},
  url = {https://doi.org/10.5114/bta/223960},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Prosopis africana protects against heavy metal mixture-induced pulmonary and hematological toxicity via nuclear factor erythroid 2-related factor 2/ nuclear factor-kappa B/ caspase-3 signaling
AU  - Harrison A. Ozoani
AU  - Kenneth O. Okolo
AU  - Baridoo Donatus Dooka
AU  - Cecilia N. Obasi
AU  - Prosper Manu Abdulai
AU  - Orish E. Orisakwe
PY  - 2026
DA  - 2026/09/09
JO  - BioTechnologia
DO  - 10.5114/bta/223960
UR  - https://doi.org/10.5114/bta/223960
AB  - Background: Heavy metal mixture (HMM) exposure poses severe health risks by inducing oxidative stress and inflammation. The limitations of conventional chelation therapy necessitate exploring natural alternatives. Although Prosopis africana (PA) has antioxidant properties, its potential as a protective agent remains underexplored. This study investigated the protective mechanisms of PA against lead/ cadmium/arsenic-induced pulmonary and hematological toxicity.  Materials and methods: Rats were treated with HMM alone or combined with PA (500, 1000, or 1500 mg/kg). The evaluated parameters included lung and blood metal accumulation, oxidative stress markers (malondialdehyde, nitric oxide), antioxidant defenses (superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase), inflammatory cytokines (interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α]), transcription factors (nuclear factor erythroid 2-related factor 2 [Nrf2], nuclear factor kappa B [NF-κB]), caspase-3, hematological parameters, and lung histopathology. Multivariate analyses were applied to integrate biomarker patterns.  Results: HMM exposure significantly increased tissue metal levels, oxidative stress, inflammatory mediators, and caspase-3 activity, while suppressing antioxidant defenses and disrupting hematological parameters and lung architecture. PA co-treatment reversed these changes in a dose-dependent manner. At 1500 mg/kg, PA reduced blood metal levels by > 90%, normalized the oxidative-antioxidant balance, decreased IL-6 and TNF-α by 60–70%, suppressed caspase-3 activity by 90%, restored hematological indices, and ameliorated lung damage. Principal component and hierarchical cluster analyses clearly separated the HMM-exposed groups from the PA-treated groups based on their distinct oxidative, inflammatory, and protective profiles.  Conclusions: PA protects against HMM-induced toxicity by reducing metal bioavailability – potentially via chelation and/or altered absorption or excretion – coupled with Nrf2 activation and NF-κB/caspase-3 suppression. These findings suggest its potential as an adjunct therapy for heavy metalinduced pathologies.
SN  - 0860-7796
SN  - 2353-9461
ER  -