GUT INTEGRITY AND BIOCHEMICAL CHANGES IN Drosophila melanogaster  EXPOSED TO CADMIUM WITH KOLAVIRON

Drosophila melanogaster shares similar biological gut mechanisms with humans, especially the midgut, which is responsible for enzymatic digestion and absorption. Cadmium, a toxic heavy metal, has been documented to cause gastrointestinal damage in humans and experimental models of rodents. Kolaviron has been reported to ameliorate several toxicities related to heavy metals in rats.  However, there is a dearth of information regarding the activities of Cadmium and kolaviron on the gut of D.melanogaster. In this work, cadmium activities in Drosophila melanogaster and its gut are observed, and the ameliorative roles of kolaviron are established. About 2000 Oregon strain of D. melanogaster (1-3 days old) were used in this study. They were grouped into four in five replicates: cadmium (0.20 mM), kolaviron (100 mg/kg diet), and cadmium and kolaviron. They were counted daily for nine days to determine their survival in the medium. After the exposure, the flies were homogenised and centrifuged to derive supernatants used to determine protein carbonyl (PC), nitric oxide (NO), lipid peroxidation (LPO), total thiol (TT) levels, catalase (CAT) and glutathione transferase (GST) activities. About 10 flies each from each group were sorted before homogenization, and their guts were excised for Bromophenol blue assay, pH determination, H and E staining and mitochondrial mass density. Data were analysed using descriptive statistics and ANOVA at α0.05. Cadmium exposure significantly reduced the survival rate, NO and TT levels, as well as CAT and GST activities, while elevating PC and LPO levels, indicating reduction-oxidation imbalance. Functionally, cadmium disrupted intestinal barrier integrity and markedly reduced midgut acidification, suggesting compromised copper cell activity. Histology revealed epithelial disorganization, cellular degeneration, and architectural distortion of gut tissue. Furthermore, MitoTracker fluorescence demonstrated significant mitochondrial membrane depolarization in cadmium-exposed flies, confirming mitochondrial dysfunction as a central event in cadmium toxicity. Kolaviron markedly ameliorated these alterations by stabilizing antioxidant capacity, protecting gut permeability and acidification, preserving epithelial morphology, and mitochondrial fluorescence intensity.  This study highlights the therapeutic potential of kolaviron in mitigating heavy metal-induced gastrointestinal toxicity.