Mechanistic insights into the inhibition of human placental glutathione S-transferase P1-1 by abscisic and gibberellic acids: An integrated experimental and computational study.

The interactions of the classic phytohormones gibberellic acid (gibberellin A3 , GA3 ) and abscisic acid (dormin, ABA), which antagonistically regulate several developmental processes and stress responses in higher plants, with human placental glutathione S-transferase P1-1 (hpGSTP1-1), an enzyme that plays a role in endo- or xenobiotic detoxification and regulation of cell survival and apoptosis, were investigated. The inhibitory potencies of ABA and GA3 against hpGSTP1, as well as the types of inhibition and the kinetic parameters, were determined by making use of both enzyme kinetic graphs and SPSS nonlinear regression models. The structural basis for the interaction between hpGSTP1-1 and phytohormones was predicted with the aid of molecular docking simulations. The IC50 values of ABA and GA3 were 5.3 and 5.0 mM, respectively. Both phytohormones inhibited hpGSTP1-1 in competitive manner with respect to the cosubstrates GSH and CDNB. When ABA was the inhibitor at [CDNB]f -[GSH]v and at [GSH]f -[CDNB]v , Vm , Km , and Ki values were statistically estimated to be 205 ± 16 µmol/min-mg protein, 1.32 ± 0.18 mM, 1.95 ± 0.25 mM and 175 ± 6 µmol/min-mg protein, 0.85 ± 0.06 mM, 1.85 ± 0.16 mM, respectively. On the other hand, the kinetic parameters Vm , Km , and Ki obtained with GA3 at [CDNB]f -[GSH]v and at [GSH]f -[CDNB]v were found to be 303 ± 14 µmol/min-mg protein, 1.77 ± 0.13 mM, 3.38 ± 0.26 mM and 249 ± 7 µmol/min-mg protein, 1.43 ± 0.07 mM, 2.89 ± 0.19 mM, respectively. Both phytohormones had the potential to engage in hydrogen-bonding and electrostatic interactions with the key residues that line the G- and H-sites of the enzyme's catalytic center. Inhibitory actions of ABA/GA3 on hpGSTP1-1 may guide medicinal chemists through the structure-based design of novel antineoplastic agents. It should be noted, however, that the same interactions may also render fetuses vulnerable to the potentially toxic effects of xenobiotics and noxious endobiotics.

Conversations in the Gut: The Role of Quorum Sensing in Normobiosis.

An imbalance in gut microbiota, termed dysbiosis, has been shown to affect host health. Several factors, including dietary changes, have been reported to cause dysbiosis with its associated pathologies that include inflammatory bowel disease, cancer, obesity, depression, and autism. We recently demonstrated the inhibitory effects of artificial sweeteners on bacterial quorum sensing (QS) and proposed that QS inhibition may be one mechanism behind such dysbiosis. QS is a complex network of cell-cell communication that is mediated by small diffusible molecules known as autoinducers (AIs). Using AIs, bacteria interact with one another and coordinate their gene expression based on their population density for the benefit of the whole community or one group over another. Bacteria that cannot synthesize their own AIs secretly "listen" to the signals produced by other bacteria, a phenomenon known as "eavesdropping". AIs impact gut microbiota equilibrium by mediating intra- and interspecies interactions as well as interkingdom communication. In this review, we discuss the role of QS in normobiosis (the normal balance of bacteria in the gut) and how interference in QS causes gut microbial imbalance. First, we present a review of QS discovery and then highlight the various QS signaling molecules used by bacteria in the gut. We also explore strategies that promote gut bacterial activity via QS activation and provide prospects for the future.

Evaluating the feasibility of performing elective gastrointestinal cancer surgery during the COVID-19 pandemic: An observational study with 60 days follow-up results of a tertiary referral pandemic hospital.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has interfered with the treatment algorithm for patients with gastrointestinal (GIS) cancer, resulting in deferral of surgery. We presented the outcomes of our patients to evaluate whether surgery could be safely performed and followed-up without delaying any stage of GIS cancer during the pandemic. METHODS: This was an observational study of 177 consecutive patients who underwent elective GIS cancer surgery between March 11 and November 1, 2020. They were assessed regarding their perioperative and 60 days follow-up results for either surgical or COVID-19 status. Morbidity was determined according to the Clavien-Dindo classification (CDC). Continuous and categorical data were presented as median ± SD and number with percentage (%), respectively. RESULTS: The study included 44 gastric, 33 pancreatic, 40 colon, and 59 rectal cancer patients. All patients underwent surgery and received neo/adjuvant treatments without delay. The overall morbidity (CDC grade II-IV) and mortality rates were 10.1% and 3.9%, respectively. None of the patients or medical staff were infected with COVID-19 during the study period. CONCLUSION: GIS cancer surgery can be safely performed even within a pandemic hospital if proper isolation measures can be achieved for both patients and health workers. Regardless of the tumor stage, surgery should not be deferred, depending on unstandardized algorithms.

Inhibitory Effects of Artificial Sweeteners on Bacterial Quorum Sensing.

Despite having been tagged as safe and beneficial, recent evidence remains inconclusive regarding the status of artificial sweeteners and their putative effects on gut microbiota. Gut microorganisms are essential for the normal metabolic functions of their host. These microorganisms communicate within their community and regulate group behaviors via a molecular system termed quorum sensing (QS). In the present study, we aimed to study the effects of artificial sweeteners on this bacterial communication system. Using biosensor assays, biophysical protein characterization methods, microscale thermophoresis, swarming motility assays, growth assays, as well as molecular docking, we show that aspartame, sucralose, and saccharin have significant inhibitory actions on the Gram-negative bacteria N-acyl homoserine lactone-based (AHL) communication system. Our studies indicate that these three artificial sweeteners are not bactericidal. Protein-ligand docking and interaction profiling, using LasR as a representative participating receptor for AHL, suggest that the artificial sweeteners bind to the ligand-binding pocket of the protein, possibly interfering with the proper housing of the native ligand and thus impeding protein folding. Our findings suggest that these artificial sweeteners may affect the balance of the gut microbial community via QS-inhibition. We, therefore, infer an effect of these artificial sweeteners on numerous molecular events that are at the core of intestinal microbial function, and by extension on the host metabolism.

Assessing the Molecular Targets and Mode of Action of Furanone C-30 on Pseudomonas aeruginosa Quorum Sensing.

Quorum sensing (QS), a sophisticated system of bacterial communication that depends on population density, is employed by many pathogenic bacteria to regulate virulence. In view of the current reality of antibiotic resistance, it is expected that interfering with QS can address bacterial pathogenicity without stimulating the incidence of resistance. Thus, harnessing QS inhibitors has been considered a promising approach to overriding bacterial infections and combating antibiotic resistance that has become a major threat to public healthcare around the globe. Pseudomonas aeruginosa is one of the most frequent multidrug-resistant bacteria that utilize QS to control virulence. Many natural compounds, including furanones, have demonstrated strong inhibitory effects on several pathogens via blocking or attenuating QS. While the natural furanones show no activity against P. aeruginosa, furanone C-30, a brominated derivative of natural furanone compounds, has been reported to be a potent inhibitor of the QS system of the notorious opportunistic pathogen. In the present study, we assess the molecular targets and mode of action of furanone C-30 on P. aeruginosa QS system. Our results suggest that furanone C-30 binds to LasR at the ligand-binding site but fails to establish interactions with the residues crucial for the protein's productive conformational changes and folding, thus rendering the protein dysfunctional. We also show that furanone C-30 inhibits RhlR, independent of LasR, suggesting a complex mechanism for the agent beyond what is known to date.

Anti-Quorum Sensing Activity of Stevia Extract, Stevioside, Rebaudioside A and Their Aglycon Steviol.

Governments are creating regulations for consumers to reduce their sugar intake, prompting companies to increase the ratio of artificial sweeteners in their products. However, there is evidence of some deleterious effects ascribed to the aforementioned synthetic agents and therefore consumers and food manufacturers have turned their attention to natural dietary sweeteners, such as stevia, to meet their sweetening needs. Stevia is generally considered safe; however, emerging scientific evidence has implicated the agent in gut microbial imbalance. In general, regulation of microbial behavior is known to depend highly on signaling molecules via quorum sensing (QS) pathways. This is also true for the gut microbial community. We, therefore, evaluated the possible role of these stevia-based natural sweeteners on this bacterial communication pathway. The use of a commercial stevia herbal supplement resulted in an inhibitory effect on bacterial communication, with no observable bactericidal effect. Purified stevia extracts, including stevioside, rebaudioside A (Reb A), and steviol revealed a molecular interaction, and possible interruption of Gram-negative bacterial communication, via either the LasR or RhlR receptor. Our in-silico analyses suggest a competitive-type inhibitory role for steviol, while Reb A and stevioside are likely to inhibit LasR-mediated QS in a non-competitive manner. These results suggest the need for further safety studies on the agents.

Computational and experimental studies on the interaction between butyrylcholinesterase and fluoxetine: implications in health and disease.

Butyrylcholinesterase (BChE) is a serine esterase that plays a role in the detoxification of natural as well as synthetic ester-bond-containing compounds. Alterations in BChE activity are associated with a number of diseases. Cholinergic system abnormalities in particular are correlated with the formation of senile plaques in Alzheimer's disease (AD), and administration of cholinesterase inhibitors is a common therapeutic approach used to treat AD. Here, our aim was to study the interaction between BChE and fluoxetine. Molecular docking simulations revealed that fluoxetine penetrated deep into the active-site gorge of BChE and that it was engaged in stabilizing noncovalent interactions with multiple subsites. In substrate kinetic studies, the Vm, Km, kcat and kcat/Km values were found to be 20.59 ± 0.36 U mg-1 protein, 194 ± 14 µM, 1.3 × 108 s-1 and 6.7 × 105 µM-1s-1, respectively. Based on inhibitory studies, fluoxetine appeared to inhibit BChE competitively, with an IC50 value of 104 µM and a Ki value of 36.3 ± 4.7 µM. Overall, both the low Ki value and the high number of BChE-fluoxetine interactions suggest that fluoxetine is a potent inhibitor of BChE, although in vivo mechanisms for the direct effects of BChE inhibition on various pathologies remain to be further investigated.

Mechanistic and structural insights into the in vitro inhibitory action of hypericin on glutathione reductase purified from baker's yeast.

This work aims at studying the interaction between glutathione reductase (GR) and hypericin. The type of inhibition was determined by measuring changes in GR activity at increasing concentrations of hypericin as well as at varying concentrations of glutathione disulfide (GSSG) and nicotinamide adenine dinucleotide phosphate (NADPH), and the binding pose of hypericin was predicted by molecular docking. Accordingly, hypericin emerges as an effective inhibitor of GR. When the variable substrate is GSSG, the type of inhibition is competitive. When the variable substrate is NADPH, however, the type of inhibition appears to be linear mixed-type competitive. Our computational analyses suggest that hypericin binds in the large intermonomer cavity of GR, and that it may interfere with the normal positioning/functioning of the redox-active disulfide center at the enzyme's active site. Overall, besides its contributory role in promoting oxidative stress via the formation of reactive oxygen species in photodynamic therapy, hypericin can also weaken cancer cells through inhibiting GR.

Evaluation of the inhibitory effect of abamectin on mammalian butyrylcholinesterase: Enzyme kinetic and molecular docking studies.

Abamectin, a blend of the natural avermectins B1a and B1b, is a widely-used insecticide/miticide with relatively low toxicity to mammals. Exposure to high doses of it, however, leads to cholinergic-like neurotoxic effects. Butyrylcholinesterase, which is best known for its abundant presence in plasma, is a serine hydrolase loosely coupled with the cholinergic system. It protects and supports the neurotransmitter function of its sister enzyme acetylcholinesterase. Here, using experimental and computational studies, we provide evidence demonstrating that abamectin is a potent (IC50 = 10.6 µM; Ki = 2.26 ± 0.35 µM) inhibitor of horse serum butyrylcholinesterase and that it interacts with the enzyme in a reversible, competitive manner predictively to block the mouth of the active-site gorge of the enzyme and to bind to several critical residues that normally bind/hydrolyze choline esters.

Fluoxetine-induced toxicity results in human placental glutathione S-transferase-π (GST-π) dysfunction.

CONTEXT: The antidepressant drug fluoxetine (FLU) is considered in the group of selective serotonine re-uptake inhibitors. Its distribution in brain and binding to human brain glutathione S-transferase-π (GST-π) have been shown. FLU can cross blood brain barrier and placenta, accumulate in fetus and may cause congenital malformations. OBJECTIVE: To elucidate the interaction of placental GST-π with FLU. MATERIALS AND METHODS: First, concentration-dependent inhibition of human placental GST-π was evaluated by using different FLU concentrations and then 0.3125, 0.625, 1.25, 2.5 and 5 mM FLU concentrations were chosen and tested while keeping GSH concentration constant and 1-chloro-2,4-dinitrobenzene (CDNB) concentration varied and vice versa. The data were evaluated with different kinetic models and Statistica 9.00 for Windows. RESULTS: The Vm, at variable [CDNB] (142 ± 16 U/mg protein) was 3 times higher than the Vm obtained at variable [GSH] (49 ± 4 U/mg protein). On the other hand, the Km for CDNB was ∼10 times higher than the Km for GSH (1.99 ± 0.36 mM versus 0.21 ± 0.06 mM). The IC50 value for FLU was 8.6 mM. Both at constant [CDNB] and variable [GSH] and at constant [GSH] and variable [CDNB] the inhibition types were competitive with the Ki values of 5.62 ± 4.37 and 8.09 ± 1.27 mM, respectively. CONCLUSION: Although the Ki values obtained for FLU in vitro are high, due to their uneven distribution, long elimination time and inhibitory behavior on detoxification systems, it may cause defects in adults but these effects may be much more severe in fetus and result in congenital malformations.

Amitriptyline may have a supportive role in cancer treatment by inhibiting glutathione S-transferase pi (GST-π) and alpha (GST-α).

A tricyclic anti-depressant, amitriptyline, is a highly prescribed drug for cancer patients for mood elevation but there are limited studies about the interaction of amitriptyline with glutathione S-transferases pi (GST-π) and glutathione S-transferases alpha (GST-α). GST isozymes have been implicated in chemotherapeutic drug resistance. We demonstrated that the concentration dependent inhibition of GST-π and GST-α by amitriptyline followed inverse hyperbolic inhibition curves with IC(50) values of 5.54 and 8.32 mM, respectively. When the varied substrate was GSH, amitriptyline inhibited both isozymes competitively and similar K(i) values were found for GST-π (K(i) = 1.61 ± 0.17 mM) and GST-α (K(i) = 1.45 ± 0.20 mM). On the other hand, when the varied substrate was CDNB, the inhibition types were non-competitive for GST-π (K(i) = 1.98 ± 0.31 mM) and competitive for GST-α (K(i) = 1.57 ± 0.16 mM). Amitriptyline, in addition to its antidepressant effect, might also have a minor supportive role on the effectiveness of the anticancer drugs by decreasing their elimination through inhibiting GST-π and GST-α.

Gastric cancer diagnosis and staging in coronavirus disease 2019 (Covid-19) pandemic.

AIM: The aim of the study was to analyze whether COVID-19 cause a delay in the diagnosis of gastric cancer patients particularly in the TNM staging of the tumor, or not. MATERIAL AND METHODS: This retrospective single-center study included the patients diagnosed with gastric cancer from March, 2019 to December 2020. The patients were divided into two groups: baseline and the pandemic groups. The following parameters were compared between the groups; demographic data, numbers of newly diagnosed patients, type of the surgery, location of the tumor, frequency of neoadjuvant treatment, ASA score, length of hospital stay, clinical staging and pathologic TNM staging. RESULTS: The mean monthly number of newly diagnosed gastric cancer patients showed a significant decline from 7.5 to 5.6 (p< .001). There were no statistically significant differences between the groups with regard to the demographic factors, except CA 19-9 levels. Patients in the pandemic group had higher both clinical and pathological T-stages (p < 0.05). CONCLUSIONS: Our study showed a decline in the number of the newly diagnosed patients with gastric cancer during the pandemic and also more patients presented with advanced stage during the pandemic period. This study showed that the pandemic causes a potential delay in the diagnosis of gastric cancer patients. KEY WORDS: Cancer surgery, COVID-19, Gastric cancer, Gastric surgery SARS-COV-2, Pandemic.

Digital Necrosis Due to Septic Embolism: An Unseen Complication of Gangrenous Cholecystitis.

Gangrenous cholecystitis is one of the most severe complications of cholelithiasis. It causes serious morbidity and mortality. The main pathology in this complication is progressive vascular insufficiency, which may lead to necrosis and perforation of the gallbladder wall. Vascular insufficiency can affect other organs besides the gallbladder. Since its symptoms are not different from that of acute cholecystitis, delayed diagnosis and treatment can cause death. Treatment is a surgical intervention as soon as the diagnosis is made. Complications such as wound infection, intra-abdominal abscess, circulatory disorders, and lung problems can be seen in the postoperative period. Embolism and necrosis in distant organs as a complication of gangrenous cholecystitis have not been reported till date. In this case, we present a patient, who developed necrosis of the fingers and toes due to septic embolism as a complication of gangrenous cholecystitis. Key Words: Cholelithiasis, Acute cholecystitis, Gangrene, Necrosis.

Duodenal Ulcer Perforation after Activated Charcoal Treatment.

Activated charcoal, having the capacity to absorb substances with its porous surface, has been used in intoxication treatment for nearly 200 years. Although live-saving, occasionally, it can lead to complications. Because of the risk of perforation during activated charcoal therapy, the integrity of the gastrointestinal tract should be checked after the procedure. In this case report, a 27-year patient, who received activated charcoal therapy after diclofenac intoxication developed duodenal ulcer perforation and charcoal peritonitis. The present case constitutes the first report of duodenal ulcer perforation after activated charcoal therapy. It should be remembered that activated charcoal, which is widely used in intoxication treatment, may cause gastrointestinal system perforation, peritonitis, adhesion, abscess formation, organ loss within the abdomen, and prolonged hospitalization. Key Words: Activated charcoal, Intoxication, Duodenal ulcer perforation.

The inhibition characteristics of human placental glutathione S-transferase-π by tricyclic antidepressants: amitriptyline and clomipramine.

Tricyclic antidepressants (TCAs) are the non-selective amine re-uptake inhibitors, well absorbed from small intestine, cross the blood-brain barrier, distributed in the brain, and are bound to glutathione S-transferase-π (GST-π). TCAs can pass through placenta, accumulate in utero baby, and cause congenital malformations. Thus, the study of the interaction of GST-π with antidepressants is crucial. In this study, the interaction of GST-π with amitriptyline and clomipramine was investigated. The K (m) values for glutathione (GSH) and 1-chloro-2,4-dinitrobenzene (CDNB) were found to be 0.16 ± 0.04 and 3.60 ± 1.67 mM, respectively. The V (m) values were varying according to the fixed substrate; [CDNB] fixed, 53 ± 3 and [GSH] fixed 182 ± 63 U/mg protein. At variable [GSH] and variable [CDNB], the k (cat) values of 7.0 × 10(6) and 1.42 × 10(7) s(-1) and the k (cat)/K (m) values of 4.38 × 10(10) and 3.94 × 10(9 )M(-1 )s(-1) were obtained, respectively. At fixed [CDNB] and variable [GSH], amitriptyline (K (s) = 0.16 ± 0.03 mM; α = 2.08; and K (i) = 1.75 ± 0.37 mM) and clomipramine (K (s) = 0.24 ± 0.05 mM; α = 1.57; and K (i) = 3.90 ± 2.26 mM) showed linear mixed-type inhibition whereas when the varied substrate is CDNB, amitriptyline (K (i) = 4.90 ± 0.68 mM) and clomipramine (K (i) = 3.37 ± 0.39 mM) inhibition were noncompetitive. The inhibition of GST-π by TCAs means the destruction of its protective role against toxic electrophiles. The effect of antidepressants on fetus will be much severe, thus, the antidepressant therapy of pregnant women should be done with caution.

Comparison of hemostatic efficacy of topical Ankaferd Blood Stopper on heparinized and nonheparinized rats in bleeding related to liver injury.

PURPOSE: In this study, hemostatic efficacy of Ankaferd Blood Stopper (ABS), a new generation hemostatic agent, was compared in the presence of heparin effect. METHODS: Forty-eight Wistar albino rats were divided into two main groups as heparinized and nonheparinized, and these two main groupswere divided into six subgroups as control, Surgicel and ABS (n = 8). Grade 2 liver injury was performed on rats as standard. All groups were compared in terms of weight, laceration surface area, prothrombin time (PT), activated partial thromboplastin time (aPTT), international normalized ratio (INR), bleeding time, bleeding amount, hemoglobin (Hb) levels, macroscopic and microscopic reactions to the agent used. RESULTS: Whereas there was no statistically significant difference between weight, laceration surface area, PT, INR and preoperative Hb values in the heparinized and nonheparinized groups, postoperative Hb, bleeding time, bleeding amount and aPTT values were statistically different (p < 0.05). In the heparin-hemostat interaction, the ABS group had the lowest bleeding in the heparinized group in terms of the amount of bleeding compared to the control and Surgicel groups (F = 0.764; p = 0.047). In macroscopic and microscopic comparison, there was no difference between the groups in terms of cell necrosis andfresh bleeding (p > 0.05), it was found that the Surgicel group had statistical significantly higher reaction scores (p < 0.05) than the other groups in terms of other parameters. CONCLUSIONS: Ankaferd Blood Stopper can be safely and effectively used in surgical practice and in patients with additional diseases requiring heparinization, since it causes minimal reaction in the liver and decreases the amount of bleeding especially in the heparinized group.

Littoral Cell Angioma of the Spleen presenting with Thrombocytosis and Splenic Infarct.

Littoral cell angioma is a non-hematologic vascular neoplasm originating from littoral cells lining the splenic red pulp. The diagnosis is usually made incidentally in splenectomy materials. It is often associated with anemia and thrombocytopenia, indicative of hypersplenism. We, herein present a case of symptomatic littoral cell angioma in a 32-year female, presumed to be accompanied by a hematologic malignancy manifesting with splenic infarct and thrombocytosis. Key Words: Littoral cell angioma, Splenic infarct, Thrombocytosis.

Correlation of Breast Cancer Subgroups and Axillary Metastases with 18F-FDG PET/CT and the Contribution of 18F-FDG PET/CT in the Management of the Axilla.

OBJECTIVE: To investigate whether breast and axilla maximum standard uptake (SUVmax) values contribute to the treatment approach in breast cancer subgroups. STUDY DESIGN: A descriptive study. PLACE AND DURATION OF STUDY: University of Health Sciences/Adana City Training and Research Hospital, Turkey, from April 2017 to September 2019. METHODOLOGY: Ninety patients, operated for early breast cancer, were examined histopathologically and demographically. Those patients were divided into subgroups, according to the St. Gallen consensus. Breast and axillary SUVmax uptakes of these subgroups were determined using (Fluorine18 fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT). These values were compared with postoperative pathology results Results: The triple negative group had the highest values and the Luminal B pos (+) group had the lowest values, when the mean values of breast and axilla SUVmax were compared. Axilla SUVmax value in those with metastatic lymph node was 1.939 times higher than those without it. The cut-off value of SUVmax value of the axillary lymph nodes was found to be 1.1 in distinguishing metastatic from non-metastatic. CONCLUSION: As the biological aggressiveness of tumor increased, SUVmax values increased in parallel. As a result, SUVmax values guided in determining the presence of axillary metastasis and treatment strategy. Key Words: Breast cancer, 18F-FDG PET/ CT, SUVmax values, Tumor subgroups, Axilla.

The Role of Ca 19-9, Ca 72-4, Cea and Cholesterol Levels in Predicting Malignancy in Gallbladder Polyps.

OBJECTIVE: To determine the association of malignancy potential of gallbladder polyps with tumor markers and cholesterol levels, and at which value the presence of malignancy should be suspected. STUDY DESIGN: Observational study. PLACE AND DURATION OF STUDY: University of Health Sciences, Adana City training and research Hospital from December 2017 to November 2020. METHODOLOGY: Ninety patients diagnosed with gallbladder polyp by abdominal ultrasonography, were included in the study. Patients were divided into subgroups of true pseudopolyp, cholesterol-non-cholesterolpolyp, malignant-non-malignant polyp. The groups were compared in terms of age, gender, polyp size, number of polyps, preoperative total cholesterol, HDL (high-density lipoprotein), LDL (low-density lipoprotein), triglyceride, Ca 19-9 (carbohydrate antigen 19-9), Ca 72-4 (carbohydrate antigen 72-4), Cea (carcinoembryonic antigen) levels. RESULTS: In the true polyp group, polyp size, Ca 19-9, Ca 72-4 and Cea median values were significantly higher (p=0.001, p=0.029, p=0.003, and p=0.007, respectively); whereas, triglyceride levels were significantly lower compared to the pseudopolyp group (p=0.002). Polyp size was significantly lower in cholesterol polyp group compared to non-cholesterol polyp group (p= 0.032), and LDL and triglyceride medians were significantly higher (p=0.031, and p<0.001) in cholesterol group. Among the true polyps, polyp size, Ca 19-9, Ca 72-4 and Cea levels were significantly higher in adenocarcinoma group than non-malignant polyp groups (p<0.05). Cut-off values were determined as >11 mm AUC: 0.906 for size, >24.1 U/mL. AUC: 1.00 for Ca 19-9, >9.6 U/mL AUC: 1.00 for Ca 72-4, and >40 ng/mL AUC: 0.984 for CEA, respectively. CONCLUSION: Polyps larger than 11mm with high levels of CEA, Ca 72-4, Ca 19-9, evaluated together, may act as a guide for the clinician in predicting malignancy. The availability of economical and accessible parameters may allow a new algorithm to be developed in the treatment and follow-up approach of gallbladder polyps. Key Words: Gallbladder polpys, Ca 19-9 antigen, Ca 72-4 antigen, Tumor marker, Gallbladder cancer.