Effect of fentanyl and remifentanil on neuron damage and oxidative stress during induction neurotoxicity.
Ali TaghizadehghalehjoughiMuhammet Emin NaldanYesim YeniSidika GencAhmet HacimuftuogluMesut IşıkAdem Necipİsmail BolatSerkan YildirimSukru BeydemirMahmut BaykanPublished in: Journal of cellular and molecular medicine (2024)
Opioids can be used for medical and non-medical purposes. Chronic pain such as cancer, as well as the frequent use of such drugs in places such as operating rooms and intensive care units, and in non-medical areas like drug abuse the effects and side effects of these drugs need to be examined in more detail. For this purpose, the effects of fentanyl and remifentanil drugs on neuroinflammation, oxidative stress and cholinesterase metabolism were investigated. Neuron cells (CRL-10742) were used for the evaluation of the toxicity of fentanyl and remifentanil. MTT, PON1 activity and total thiol levels for its effect on oxidative stress, AChE and BChE activities for its effect on the cholinergic system, and TNF, IL-8 and IL-10 gene levels for its neuroinflammation effect were determined. The highest neurotoxic dose of fentanyl and remifentanil was determined as 10 μg/mL. It was observed that the rate of neuron cells in this dose has decreased by up to 61.80% and 56.89%, respectively. The IL-8 gene expression level in both opioids was down-regulated while IL 10 gene level was up-regulated in a dose-dependent manner compared to the control. In our results, the TNF gene expression level differs between the two opioids. In the fentanyl group, it was seen to be up-regulated in a dose-dependent manner compared to the control. Fentanyl and remifentanil showed an inhibitory effect against PON1, while remifentanil showed an increase in total thiol levels. PON1, BChE and total thiol activities showed similarity with MTT.
Keyphrases
- oxidative stress
- chronic pain
- induced apoptosis
- gene expression
- pain management
- healthcare
- dna damage
- dna methylation
- transcription factor
- diabetic rats
- intensive care unit
- ischemia reperfusion injury
- cell cycle arrest
- endoplasmic reticulum stress
- traumatic brain injury
- rheumatoid arthritis
- copy number
- signaling pathway
- genome wide
- lipopolysaccharide induced
- cognitive impairment
- lps induced
- cell death
- drug induced
- cerebral ischemia
- inflammatory response
- emergency department
- genome wide identification
- subarachnoid hemorrhage
- genome wide analysis