TOXICITY

6PPD-quinone (6PPD-Q) is a transformation product of the tyre additive 6PPD. It enters aquatic systems through stormwater runoff and poses an emerging toxicological concern. This study examined the acute and sub-lethal effects of 6PPD-Q on Clarias gariepinus, a freshwater catfish commonly used in ecotoxicological studies. The objective was to determine the sensitivity of Clarias gariepinus to 6PPD-Q and to assess changes in haematological parameters as indicators of physiological stress. Juvenile Clarias gariepinus were exposed under laboratory conditions to a range of 6PPD-Q concentrations for 96 hours to evaluate acute toxicity, followed by sub-lethal exposure for haematological analysis. No mortality was recorded during the acute phase, indicating that the compound did not reach a lethal threshold within the tested concentration range. Sub-lethal exposure produced measurable haematological alterations. There was a significant decrease (P<0.05) in red blood cell count, haemoglobin concentration, and packed cell volume, suggesting anaemia and impaired oxygen transport. White blood cell counts increased, indicating immune response activation. These findings demonstrate that 6PPD-Q affects fish health at non-lethal levels, even when acute mortality is absent. This study highlights the ecological risk posed by 6PPD-Q in aquatic environments. Its persistence and sub-lethal toxicity underscore the need for environmental monitoring and regulation of tire-derived pollutants. Further research should address long-term exposure, tissue accumulation, and population-level impacts in freshwater ecosystems.

Hippocampal dysfunction, often linked to learning and memory impairments, can result from neurodegeneration or exposure to toxic agents. Manganese chloride, a neurotoxic compound, accumulates in the hippocampus and disrupts neuronal signalling through oxidative stress, mitochondrial dysfunction, and inflammation, leading to cognitive deficits. Vanillin, a natural phenolic compound with antioxidant and anti-inflammatory properties, has shown potential in protecting against such neurotoxic damage and preserving hippocampal integrity. Accordingly, the aim of this study was to evaluate the activity of vanillin on manganese chloride-induced hippocampal toxicity in Wistar rats. Forty-eight (48) adult Wistar rats were randomly assigned into six groups (A-F). Group A served as control; Group B received 10 mg/kg body weight [BW] of manganese chloride only; Group C received 20 mg/kg BW of vanillin and 10 mg/kg BW of manganese chloride. Group D received 40 mg/kg BW of vanillin and 10 mg/kg BW of manganese chloride. Group E received 20 mg/kg BW of vanillin only and Group F received 40 mg/kg BW of vanillin only. All administrations, lasted for twenty-eight (28) days. Nneurobehavioral activities were evaluated using the Novel object recognition and elevated plus maze tests.