Berberine Attenuates Acetamiprid Exposure-Induced Mitochondrial Dysfunction and Apoptosis in Rats via Regulating the Antioxidant Defense System.

Acetamiprid (ACMP) is a neonicotinoid insecticide that poses a significant threat to the environment and mankind. Oxidative stress and mitochondrial dysfunction are considered prime contributors to ACMP-induced toxic effects. Meanwhile, berberine (BBR) a natural plant alkaloid, is a topic of interest because of its therapeutic and prophylactic actions.

Berberine mitigates acetamiprid-induced hepatotoxicity and inflammation via regulating endogenous antioxidants and NF-κB/TNF-α signaling in rats.

Acetamiprid is a neonicotinoid insecticide used on a large scale and has been reported for oxidative stress-mediated toxicity and physiological alterations in mammals. The plant-derived natural antioxidant berberine (BBR) possesses protective potential against inflammation, structural changes, and cellular toxicity. The current study aimed to investigate the toxic effects of acetamiprid exposure and the antioxidative and anti-inflammatory efficacy of BBR in rat liver tissue.

Neuroprotective potential of berberine against acetamiprid induced toxicity in rats: Implication of oxidative stress, mitochondrial alterations, and structural changes in brain regions.

Acetamiprid (ACMP) is an extensively used neonicotinoid pesticide to control sucking and chewing insects and is known to cause nontarget toxicity. The present study aimed to evaluate the ameliorative potential of berberine (BBR)-a polyphenolic alkaloid- on ACMP-induced oxidative stress, mitochondrial dysfunctioning, and structural changes in different rat brain regions. The male Wistar rats were divided into four groups, that is, control, BBR-treated (150 mg/kg b.

N-acetylcysteine ameliorates monocrotophos exposure-induced mitochondrial dysfunctions in rat liver.

Monocrotophos (MCP) is an organophosphate pesticide with well-known toxicity in mammals. Exposure of MCP is associated with altered molecular physiology at sub-cellular levels. This study investigated the efficacy of -acetylcysteine (NAC) against MCP exposure mediated mitochondrial dysfunctions in hepatic tissue of rats.

-Acetylcysteine Reverses Monocrotophos Exposure-Induced Hepatic Oxidative Damage via Mitigating Apoptosis, Inflammation and Structural Changes in Rats.

Oxidative stress-mediated tissue damage is primarily involved in hepatic injuries and dysfunctioning. Natural antioxidants have been shown to exert hepatoprotective, anti-inflammatory and antiapoptotic properties. The present study evaluated the effect of -acetylcysteine (NAC) against monocrotophos (MCP) exposure-induced toxicity in the rat liver.