Clomazone-based commercial herbicide causes systemic alterations in Wistar rats after repeated exposure.
TL;DR
Overall, clomazone exposure produced dose-dependent neurochemical, renal, hepatic, and adrenal effects, revealing that even subchronic exposure can alter redox homeostasis and cellular integrity.
Abstract
Clomazone is a widely used herbicide with reported toxicity in target and non-target species. This study investigated its subchronic effects in adult male rats treated orally with 15, 30, or 60 mg/kg for 28 days. A control group received distilled water. Behavioral, biochemical, hematological, and histopathological parameters were evaluated, along with markers of oxidative stress and DNA damage. Rats treated with 60 mg/kg showed increased grooming behavior, suggesting neurobehavioral alterations. Kidney evaluation revealed decreased relative organ mass at 60 mg/kg and increased non-protein thiols at 15 mg/kg, indicating oxidative responses. In the liver, mitochondrial complex IV activity increased at 30 mg/kg, suggesting mitochondrial adaptation. Elevated GABA levels were detected in the hippocampus and hypothalamus at 60 mg/kg, consistent with potential neurotoxicity. Histopathological analysis showed adrenal damage characterized by hydropic and hyaline degeneration, apoptosis and necrosis. No major hematological or overt systemic toxicity was observed. Overall, clomazone exposure produced dose-dependent neurochemical, renal, hepatic, and adrenal effects, revealing that even subchronic exposure can alter redox homeostasis and cellular integrity. These findings reinforce the need for careful risk assessment and monitoring of clomazone exposure to prevent potential neurotoxic and nephrotoxic effects.