Subchronic exposure to T-2 toxin triggered neurobehavioral damage in developing juvenile rats was associated with oxidative stress and mitochondrial pathway-induced apoptosis of hippocampal neurons

T-2 toxin represents a significant hazard to animal husbandry and human health. Studies have shown that T-2 toxins are able to induce neurotoxicity by disrupting the blood-brain barrier or by inducing neuronal dysfunction. And during the developmental period, a critical period for neurological development, the neurotoxic effects produced after exposure to T-2 toxins have not yet been fully elucidated. This study was concentrated on the neurotoxic impacts of T-2 toxin on hippocampus neurons using juvenile male Wistar rats as an experimental model. Through behavioral assessments, Hematoxylin-Eosin (HE) staining, Nissl staining, and transmission electron microscopy (TEM), we evaluated hippocampal pathological damage and its correlation with behavioral alterations. To elucidate the underlying mechanisms, we analyzed oxidative stress markers, including reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD). We also detected mitochondrial membrane potential, hippocampus neuronal apoptosis, and associated protein and mRNA expression levels (Bax, Bcl-2, Caspase-3). These findings imply that (1) T-2 toxin exposure induced neurobehavioral deficits and hippocampus structural damage; (2) T-2 toxin triggered oxidative stress within the rat's hippocampus, characterized by suppressed SOD activity alongside upregulated ROS and MDA levels; and (3) T-2 toxin disrupted mitochondrial function, leading to increased neuronal apoptosis and altered expression of apoptosis-associated proteins and mRNA. These findings give an in-depth understanding of the molecular mechanisms by which T-2 toxin exerts neurotoxic effects. Offering a theoretical foundation for developing targeted therapeutic interventions.