Evidence map›Paper›PMID 40268769›Full record

ArticleBiological trace element research2025

Gastrointestinal-Ocular Toxicity Following Systematic Ingestion of Nickel-Cadmium Contaminated Water in Wistar Rats Demonstrates Possible Health Complications Characterized by Oxidative Stress, Inflammatory and Histological Changes.

Chiedu Onyinye Emeninwa, Augustine Apiamu, Samuel Ogheneovo Asagba

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Article in Biological trace element research, 2025. 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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1 · What the graph read from it

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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.

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5 · Who and what money

Authors and funding

3 authors.

Chiedu Onyinye EmeninwaDepartment of Biochemistry, Faculty of Science, Delta State University of Science and Technology, Ozoro, Nigeria. chiemeninwa@gmail.com.
Augustine ApiamuDepartment of Biochemistry, Faculty of Science, Delta State University, Abraka, Nigeria.
Samuel Ogheneovo AsagbaDepartment of Biochemistry, Faculty of Science, Delta State University, Abraka, Nigeria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The study evaluated the biochemical and histopathological alterations of subacute nickel (Ni) and cadmium (Cd) exposure on the gastrointestinal and ocular systems of male Wistar albino rats via ingestion of contaminated water. Four groups of six rats each were exposed to uncontaminated water (group A as control), 100 mg/L of Cd (group B), 100 mg/L of Ni (group C), and a combination of 100 mg/L Cd and Ni (group D) for 28 days. The stomach, intestinal, and ocular weights were recorded and were significantly reduced (p ≤ 0.05) in the treatment groups when compared to the control, but the effect was profound in group D rats, as compared with groups B and C rats. The assessed amylase, lipase, and alkaline phosphatase (ALP) activities were significantly impaired (p > 0.05) in the tissues with some exceptions among treatment groups relative to the control. The increased stomach, intestinal, and ocular malondialdehyde (MDA) levels (p ≤ 0.05) affirmed the induction of oxidative stress among treatment groups with depleted antioxidant defense system in assessed tissues, but no significant change (p > 0.05) in ocular reduced glutathione (GSH) level was observed, as compared with the control. The tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) levels assessed were significantly elevated (p ≤ 0.05) in the tissues of groups B and D rats with some exceptions among group C rats when compared to the control. The histological alteration characterized by cellular degeneration, oxidative damage, inflammation, and tissue necrosis further affirmed the synergistic impacts with indications of gastritis, retinal dysfunction, and ocular impairment in predisposed rats.

Indexed as

CadmiumEyeGastrointestinal TractInflammationNickelOxidative StressWater Pollutants, ChemicalAnimalsMaleRatsRats, WistarCadmiumNickelWater Pollutants, ChemicalCadmiumGastritisInflammationNickelOxidative stressRetinal dysfunction

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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 OpenQuestion graph.