2 research outputs found
Pro-Neurogenic and Antioxidant Efficacy of Nigella sativa Oil Reduced Vulnerability Cholinesterase Dysfunction and Disruption in Amygdala-Dependent Behaviours in Chlorpyrifos Exposure
Background: Organophosphorus Pesticides (OPs) are
compounds with irreversible cholinesterase activity
which induce cholinergic neurotoxicity, but still remain
a widely used pesticide in household and agriculture.
Aim and Objectives: This study investigated the
efficacy of a natural antioxidant Nigella sativa Oil
(NSO) against Chlorpyrifos (CPF) induced oxidative
stress and implications on emotionality behaviours.
Material and Methods: Thirty-two adult Wistar rats
were randomly divided into four groups, and exposed
to (1 ml/kg b w) of normal saline, (14.9 mg/kg b w) of
CPF, (14.9 mg/kg b w) of CPF plus (1 ml/kg b w) of
NSO and (1 ml/kg b w) of NSO respectively for 14
consecutive days. Body weight were recorded at day 1
and 15 of the experiment, the rats were exposed to trials
in both Open Field Test (OFT) and Elevated Plus Maze
(EPM) to asses anxiety-like behaviours and fear related
learning respectively on the 13th day. Rats were
euthanized by the 15th day, the brains excised, and the
amygdala area of brains were removed, homogenized
to analyse for total Reactive Oxygen Species (ROS),
Nitrous Oxide (NO) levels and Acetylcholinesterase
(AChE) activities, while the other three were processed
for histology (Nissl stain) and Proliferative marker
(Ki67 immunohistochemistry). Results: Repeated CPF
exposure caused an increase in NO and ROS levels,
reduction in AChE activities and a loss in the
neurogenic cells in the amygdala. It was also a
prolonged freezing period, centre squares avoidance
and delayed transfer latency with CPF exposure.
However, NSO prevented the overproduction of ROS
and NO, and markedly reactivated AChE activities in
the amygdala either with or without CPF exposure.
NSO treatment was also, able to preserve neurogenic
cells in the amygdala and subsequently improved
amygdala-dependent behaviours in the treated rats.
Conclusion: The antioxidant efficacy of NSO could be
efficacious in CPF induced neuro-cognitive toxicity in
rats
Chlorpyrifos- and Dichlorvos-Induced Oxidative and Neurogenic Damage Elicits Neuro-Cognitive Deficits and Increases Anxiety-Like Behavior in Wild-Type Rats
The execution of agricultural activities on an industrial scale has led to indiscriminate deposition of toxic xenobiotics, including organophosphates, in the biome. This has led to intoxication characterized by deleterious oxidative and neuronal changes. This study investigated the consequences of oxidative and neurogenic disruptions that follow exposure to a combination of two organophosphates, chlorpyrifos (CPF) and dichlorvos (DDVP), on neuro-cognitive performance and anxiety-like behaviors in rats. Thirty-two adult male Wistar rats (150⁻170 g) were randomly divided into four groups, orally exposed to normal saline (NS), DDVP (8.8 mg/kg), CPF (14.9 mg/kg), and DDVP + CPF for 14 consecutive days. On day 10 of exposure, anxiety-like behavior and amygdala-dependent fear learning were assessed using open field and elevated plus maze paradigms, respectively, while spatial working memory was assessed on day 14 in the Morris water maze paradigm, following three training trials on days 11, 12, and 13. On day 15, the rats were euthanized, and their brains excised, with the hippocampus and amygdala removed. Five of these samples were homogenized and centrifuged to analyze nitric oxide (NO) metabolites, total reactive oxygen species (ROS), and acetylcholinesterase (AChE) activity, and the other three were processed for histology (cresyl violet stain) and proliferative markers (Ki67 immunohistochemistry). Marked (p ≤0.05) loss in body weight, AChE depletion, and overproduction of both NO and ROS were observed after repeated exposure to individual and combined doses of CPF and DDVP. Insults from DDVP exposure appeared more severe owing to the observed greater losses in the body weights of exposed rats. There was also a significant (p ≤0.05) effect on the cognitive behaviors recorded from the exposed rats, and these deficits were related to the oxidative damage and neurogenic cell loss in the hippocampus and the amygdala of the exposed rats. Taken together, these results provided an insight that oxidative and neurogenic damage are central to the severity of neuro-cognitive dysfunction and increased anxiety-like behaviors that follow organophosphate poisoning