Effect of fentanyl and remifentanil on neuron damage and oxidative stress during induction neurotoxicity
Neurons
0303 health sciences
Aryldialkylphosphatase
Interleukin-8
Original Articles
Fentanyl
Remifentanil
Analgesics, Opioid
Oxidative Stress
03 medical and health sciences
Piperidines
Neuroinflammatory Diseases
Humans
Sulfhydryl Compounds
Chronic Pain
DOI:
10.1111/jcmm.18118
Publication Date:
2024-02-09T05:34:37Z
AUTHORS (11)
ABSTRACT
AbstractOpioids 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.
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