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.

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.