Carbamate compounds induced toxic effects by affecting Nrf2 signaling pathways.

Carbamate (CBs) is a class of insecticides which is being known as an important cause of intentional or accidental poisoning. CBs, cause carbamylation of acetylcholinesterase at neuronal synapses and neuromuscular junction. Exposure to CBs through skin contact, inhalation, or ingestion can result in significant cholinergic toxicity. This is due to the elevation of acetylcholine levels at ganglionic synapses found in both the sympathetic and parasympathetic nervous systems, as well as muscarinic receptors located in target organs of the parasympathetic nervous system, nicotinic receptors situated in skeletal muscle tissue, and the central nervous system. The association between human illnesses and environmental exposures to CBs have been extensively studied in several studies. Although CBs-triggered toxicity leads to overproduction of reactive oxygen species (ROS), the detailed association between the toxicity under CBs exposure and NFE2-related factor 2 (Nrf2) signaling pathways has not been completely clarified. In this review we aimed to summarize the latest findings on the functional interrelationship between carbamates compounds and Nrf2 signaling.

Involvement of Nrf2 signaling in lead-induced toxicity.

Nuclear factor erythroid 2-related factor 2 (Nrf2) is used as one of the main protective factors against various pathological processes, as it regulates cells resistant to oxidation. Several studies have extensively explored the relationship between environmental exposure to heavy metals, particularly lead (Pb), and the development of various human diseases. These metals have been reported to be able to, directly and indirectly, induce the production of reactive oxygen species (ROS) and cause oxidative stress in various organs. Since Nrf2 signaling is important in maintaining redox status, it has a dual role depending on the specific biological context. On the one hand, Nrf2 provides a protective mechanism against metal-induced toxicity; on the other hand, it can induce metal-induced carcinogenesis upon prolonged exposure and activation. Therefore, the aim of this review was to summarize the latest knowledge on the functional interrelation between toxic metals, such as Pb and Nrf2 signaling.