Ectoenzymes and cholinesterase activity and biomarkers of oxidative stress in patients with lung cancer

Abstract

We aimed to examine the nucleoside triphosphate diphosphohydrolases (NTPDase) in lymphocytes; adenosine deaminase (ADA) and butyrylcholinesterase (BChE) in serum; and acetylcholinesterase (AChE), superoxide dismutase (SOD), and catalase (CAT) activity in whole blood; since these enzymes are involved in inflammation responses as well as in oxidative stress conditions. We also checked the levels of total thiols (T-SH), non-protein thiols (NPSH), and thiobarbituric acid reactive substances (TBARS) in serum of patients with lung cancer. We collected blood samples from patients (n = 31) previously treated for lung cancer with chemotherapy. Patients were classified as stage IIIb and IV according to the Union for International Cancer Control (UICC). The results showed a significant increase in the hydrolysis of ATP, ADP, and adenosine in patients when compared with the control group. The activity of AChE, SOD, and CAT as well as the T-SH and NPSH levels were higher in patients group and TBARS levels were lower in patients compared with the control group. These findings demonstrated that the enzymes activity involved in the control of inflammatory and immune processes as well as the oxidative stress parameters are altered in patients with lung cancer.

Swimming training prevents alterations in ecto-NTPDase and adenosine deaminase activities in lymphocytes from Nω-nitro-L-arginine methyl ester hydrochloride induced hypertension rats

“…Taken together, these data suggest that the increased ecto-NTPDase and ADA activities in lymphocytes of hypertensive rats are occurring due to the activation of pro-inflammatory mediators. Alterations in purinergic system enzymes related to other diseases, such as lung cancer, Chagas' disease, experimental sepsis and multiple sclerosis, were already described in recent studies developed by our research group [27,40,44,45].…”

IGFBP-3 Blocks Hyaluronan-CD44 Signaling, Leading to Increased Acetylcholinesterase Levels in A549 Cell Media and Apoptosis in a p53-Dependent Manner

“…P53 is mutated in ~50% of human cancers and its function as a critical tumor suppressor and in regulation of a large number of genes involved in inhibition of cell proliferation, cell-cycle arrest, apoptosis and senescence, is well-documented 55,56,79 . Several earlier reports showed that the activity of AChE was reduced in lung cancer, likely contributing to lung cancer growth 61,[68][69][70] . Moreover, blocking AChE expression by siRNA or treatment with AChE pharmacological inhibitors, blocked apoptosis 61,71 .…”

“…While AChE is not an apoptosis initiator, it acts as a tumor suppressor, in part by the catalytic hydrolysis of acetylcholine 61,[68][69][70] . The activity of AChE was found to be reduced in lung cancer, likely contributing to increased acetylcholine levels, lung cancer growth and tumor aggressiveness, poor prognosis, and low survival rate 61,[68][69][70] . Apoptosis was prevented when using anti-sense oligonucleotides of AChE 71 .…”

Effects of Nanosilver Exposure on Cholinesterase Activities, CD41, and CDF/LIF-Like Expression in ZebraFish (Danio rerio) Larvae

“…The responses of the molecules related to the cholinergic system to inflammation have been studied thoroughly by other authors: the group of Wessler et al (e.g., [48]), the group of Soreq (e.g. [52]), and others (e.g., [53]). On the other hand, CDF/LIF, which enhances the cholinergic differentiation, is involved in the downregulation of immune cell proliferation in case of inflammation.…”