Search Results (266)

Cardiovascular disease (CVD) and dementia may share common pathogenic factors such as atherosclerosis and hyperlipoproteinemia. Dyslipidemia-induced oxidative stress contributes to dementia comorbidity in CVD. Abelmoschus esculentus (AE, okra) potentiates in alleviating hyperlipidemia and diabetes-related cognitive impairment. This study evaluated the effects of AE in hyperlipidemic ApoE^−/− mice treated with streptozotocin (50 mg/kg) and fed a high-fat diet (17% lard oil, 1.2% cholesterol). AE fractions F1 or F2 (0.65 mg/kg) were administered for 8 weeks. AE significantly reduced serum LDL-C, HDL-C, triglycerides, and glucose, improved cognitive and memory function, and protected hippocampal neurons. AE also lowered oxidative stress markers (8-hydroxy-2′-deoxyguanosine, 8-OHdG) and modulated neuronal nuclei (NeuN) and doublecortin (DCX) expression. In vitro, AE promoted neurite outgrowth and neuronal differentiation in retinoic acid (RA)-differentiated human SH-SY5Y cells under metabolic stress (glucose and palmitate), alongside the upregulation of heme oxygenase-1 (HO-1), Nuclear factor-erythroid 2-related factor 2 (Nrf2), and brain-derived neurotrophic factor (BDNF). These findings suggest AE may counter cognitive decline via oxidative stress regulation and the enhancement of neuronal differentiation. Full article

Although ART leads to viral suppression, people living with HIV (PLWH) still face an increased risk of comorbidities, such as cancer. The HIV-1 Tat protein may contribute to the promotion of chronic inflammation, oxidative stress, and genomic instability. While the presence of anti-Tat antibodies has been associated with slower disease progression, their potential role in modulating DNA damage remains unclear. Assess the effect of anti-Tat antibodies on cytotoxic and DNA damage in PLWH. A cross-sectional study was conducted in 178 PLWH. Serum anti-Tat IgG antibodies were measured using enzyme-linked immunosorbent assay (ELISA). Cytotoxicity and DNA damage were assessed via serum 8-hydroxy-2′-deoxyguanosine (8-OHdG) and nuclear anomalies (Micronucleus cytome assay) in 2000 buccal cells. Statistical significance was considered at p < 0.05. Anti-Tat antibodies were found in 24.2% of participants. Positive individuals had lower CD4+ T cell counts (p = 0.045) and higher levels of pyknosis (p = 0.0001). No differences in 8-OHdG were found, but 8-OHdG correlated positively with CD4+ counts (rho = 0.334, p = 0.006). Pyknosis negatively correlated with CD4+ counts (rho = −0.272, p = 0.027). Anti-Tat antibodies may not prevent DNA damage but could be related to cytotoxic effects in PLWH. Full article

Diabetes is the world’s leading cause of renal and premature cardiovascular disease. There are marked differences between groups of patients with different ethnicities in their susceptibility to diabetes and its renal and cardiovascular complications. Novel markers of developing diabetes complications are related to disturbances in oxidative metabolism. In this cross-sectional study, we measured the arterial stiffness in patients of differing ethnicities with type 2 diabetes mellitus and assessed the relationship of their ethnicity with systemic markers of oxidative stress. Patients from black, African and Caribbean, and Asian minor ethnic groups were studied, with white patients with T2DM (n = 170) without evidence of cardiovascular disease (CVD). The vascular stiffness was measured by infrared finger-photoplethysmography. The oxidative stress burden was assessed by measuring the urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG), activities of plasma glutathione peroxidase (GPx-3), superoxide dismutase (SOD) activities, and concentration of selenium. The vascular stiffness and 8-OHdG were higher in the white than in the Black patients (9.68 m/s vs. 9.26 m/s, p = 0.021 and 292.8 ng/mL vs. 200.9 ng/mL, p = 0.0027, respectively). Meanwhile, the GPx-3 and SOD activities and selenium were lower in the white than in the Black patients (283.3 U/L vs. 440.4 U/L, p < 0.0001; 37.5 U/L vs. 75.6 U/L, p = 0.0007; and 1.14 vs. 1.28 µmol/L, p = 0.0001, respectively). In regression modelling, the 8-OHdG/creatinine ratio was an independent predictor of vascular stiffness in the white patient group (β = 0.23 m/s per unit increase in ln(8-OHdG/creatinine) [95% CI, 0.03 to 0.42]; p = 0.021) but not in the Black patient group (p = 0.29). Increased vascular stiffness, lower endogenous antioxidant defense, and greater levels of oxidative damage were found in patients of white ethnicity, which could contribute to the higher incidence of CVD compared with patients from Black minor ethnic groups with diabetic renal disease. Full article

Ultraviolet (UV) radiation stimulates melanogenesis, leading to various esthetic problems. UV increases oxidative stress and nuclear factor-kappa B (NF-κB), which increase the nucleotide-binding oligomerization domain (NOD) or leucine-rich repeat and pyrin do-main containing 3 (NLRP3) inflammasome. Given that polydeoxyribonucleotides reduce melanogenesis and polynucleotide (PN) has molecular similarity to polydeoxyribonucleotides, we hypothesized that PN can decrease melanogenesis. We compared the anti-melanogenic effect of PN with that of a PN mixture (PNM) that contained other antioxidants, such as glutathione and hyaluronic acid, in UVB-irradiated keratinocytes and animal skin. PN and PNM both decreased oxidative stress, which was evaluated according to the expression of NADPH oxidase (NOX) 1/2/4, the glutathione (GSH):oxidized glutathione (GSSG) ratio, and 8-hydroxy-2′-deoxyguanosine (8-OHdG) in UVB-irradiated keratinocytes. The expression of NLRP3 inflammasome components (NLRP3, ASC, and pro-caspase-1) and IL-18 was increased by UVB radiation and reduced by PN and PNM. When conditioned media from PN or PNM were administered to UVB-radiated keratinocytes, melanogenesis-related signals (MITF, tyrosinase, and tyrosinase-related protein1/2) were decreased. These effects were similar in the UVB-irradiated animal skin. Both PN and PNM decreased melanin accumulation and increased skin lightness in UVB-irradiated skin. The anti-melanogenic effect of PNM was greater than that of PN. In conclusion, PN and PNM decreased melanogenesis by decreasing oxidative stress, NF-κB, and NLRP3 inflammasome activation. Full article

: Negative energy balance (NEB) in dairy cows induces excessive lipolysis, leading to elevated levels of β-hydroxybutyric acid (BHBA), which, when accumulated, can cause liver damage. Rutin (RT), a natural flavonoid with antioxidant and anti-inflammatory properties, has demonstrated potential hepatoprotective effects; however, its ability to mitigate BHBA-induced hepatocellular injury in calves remains unclear. This study first assessed the impact of various BHBA concentrations on oxidative stress in calf hepatocytes, then explored the protective effects and underlying mechanisms of RT, and finally employed untargeted metabolomics to further elucidate RT’s mode of action. The results showed that exposure to 1.2 mM BHBA significantly increased malondialdehyde (MDA), nitric oxide (NO) contents, and reactive oxygen species (ROS) levels, while markedly decreasing glutathione (GSH) content and catalase (CAT) activity compared with the blank control. Notably, pretreatment with 100 μg/mL RT resulted in the greatest increase in GSH contents (180%) compared to BHBA treatment alone, while 150 μg/mL RT led to the most pronounced reduction in MDA contents (220%). Furthermore, BHBA treatment significantly upregulated the expression of Kelch-like ECH-associated protein 1 (Keap1) and downregulated nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H quinone dehydrogenase 1 (NQO1), and heme oxygenase-1 (HO-1) at both the mRNA and protein levels. These alterations were effectively reversed by pretreatment with 100 μg/mL RT. Non-targeted metabolomics identified 1525 metabolites in total. Based on OPLS-DA, metabolites with a variable importance in projection (VIP) > 1 and p < 0.05 were considered significantly altered. Compared with the blank control, BHBA treatment upregulated 47 metabolites—including 8-hydroxy-2′-deoxyguanosine, 3-hydroxyisovaleric acid, and N-palmitoyl-sphingosine—and downregulated 58 metabolites, such as betaine, linolenic acid, and arachidonic acid. In contrast, RT pretreatment upregulated 207 metabolites relative to the BHBA treatment, including linolenic acid, taurocholic acid, and 4-hydroxybenzoic acid, and downregulated 126 metabolites, including 3-hydroxyisovaleric acid, 8-hydroxy-2′-deoxyguanosine, and pyruvaldehyde. Pathway enrichment analysis indicated that RT alleviated BHBA-induced hepatocyte injury primarily by modulating the fatty acid degradation pathway. In summary, RT mitigated BHBA-induced oxidative stress in calf hepatocytes by regulating the Keap1/Nrf2 signaling pathway and further exerted protective effects through metabolic reprogramming. Full article

Objectives: To evaluate how a 10-day multi-stressor field-training course—combining high physical and psycho-emotional demands, caloric restriction, and severe sleep deprivation—affects systemic oxidative/antioxidative status and biomarkers of nucleic-acid and skeletal-muscle damage in trained military cadets. Methods: Seventy-five healthy cadets (8 women, 67 men; 22–34 y) completed the course. Standardised operational rations (700–800 kcal day⁻¹) and two 20 min tactical naps per 24 h were enforced. Pre- and post-course venous blood was collected after an overnight fast. Plasma superoxide-dismutase activity (SOD), reduced and oxidised glutathione (GSH, GSSG), malondialdehyde (MDA), and hydrogen peroxide (H₂O₂) were quantified by colourimetric/fluorometric assays; 8-hydroxy-2-deoxyguanosine (8-OHdG) and myoglobin were measured by ELISA. The oxidative-stress index (OSI) was calculated as GSSG·GSH⁻¹. Within-subject differences were assessed with Wilcoxon signed-rank tests; associations between biomarker changes were explored by Spearman correlation. Results: After training, GSH (+175%, p < 0.001) and GSSG (+32%, p < 0.001) rose significantly, whereas SOD (−19%, p = 0.002), H₂O₂ (−20%, p = 0.015), MDA (−50%, p < 0.001), 8-OHdG (−23%, p < 0.001), and OSI (−47%, p < 0.001) declined. Myoglobin remained unchanged (p = 0.603). Reductions in MDA correlated inversely with increases in GSSG (rₛ = −0.25, p = 0.041), while H₂O₂ changes correlated positively with GSSG (rₛ = 0.25, p = 0.046), indicating a glutathione-driven adaptive response. Conclusions: Ten consecutive days of vigorous, calorie- and sleep-restricted field training elicited a favourable redox adaptation characterised by enhanced glutathione-mediated antioxidant capacity and lower circulating oxidant concentrations, without evidence of DNA or skeletal-muscle damage. The data suggest that, in physically prepared individuals, prolonged multi-stressor exposure can strengthen endogenous antioxidant defences rather than precipitate oxidative injury. Full article

Male-factor infertility accounts for nearly half of all infertility cases, and mounting evidence points to oxidative stress as a pivotal driver of sperm dysfunction, genetic instability, and epigenetic dysregulation. In particular, the oxidative DNA lesion 8-hydroxy-2′-deoxyguanosine (8-OHdG) has emerged as a central mediator at the interface of DNA damage and epigenetic regulation. We discuss how this lesion can disrupt key epigenetic mechanisms such as DNA methylation, histone modifications, and small non-coding RNAs, thereby influencing fertilization outcomes, embryo development, and offspring health. We propose that the interplay between oxidative DNA damage and epigenetic reprogramming is further exacerbated by aging in both the paternal and maternal germlines, creating a “perfect storm” that increases the risk of heritable (epi)mutations. The consequences of unresolved oxidative lesions can thus persist beyond fertilization, contributing to transgenerational health risks. Finally, we explore the promise and potential pitfalls of antioxidant therapy as a strategy to mitigate sperm oxidative damage. While antioxidant supplementation may hold significant therapeutic value for men with subfertility experiencing elevated oxidative stress, a careful, personalized approach is essential to avoid reductive stress and unintended epigenetic disruptions. Recognizing the dual role of oxidative stress in shaping both the genome and the epigenome underscores the need for integrating redox biology into reproductive medicine, with the aim of improving fertility treatments and safeguarding the health of future generations. Full article

Myocardial oxidative stress increases under conditions of hyperglycemia and ischemia/reperfusion (I/R) injury, leading to cellular damage. Inhibition of oxidative stress is involved in the cardioprotective effects of hydrogen sulfide (H₂S) during I/R and diabetes, and H₂S has the potential to protect the heart. However, the mechanism by which H₂S regulates the level of cardiac reactive oxygen species (ROS) during I/R and hyperglycemic conditions remains unclear. Therefore, the objective of this study was to evaluate the cytoprotective effect of H₂S in primary cardiomyocyte cultures subjected to hyperglycemia, hypoxia–reoxygenation (HR), or both conditions, by assessing the PPAR-α/Keap1/Nrf2/p47phox/NOX4/p-eNOS/CAT/SOD and the PPAR-γ/PGC-1α/AMPK/GLUT4 signaling pathways. Treatment with NaHS (100 μM) as an H₂S donor in cardiomyocytes subjected to hyperglycemia, HR, or a combination of both increased cell viability, total antioxidant capacity, and tetrahydrobiopterin (BH₄) concentrations, while reducing ROS production, malondialdehyde concentrations, 8-hydroxy-2′-deoxyguanosine, and dihydrobiopterin (BH₂) concentrations. Additionally, the H₂S donor treatment increased the expression and activity of PPAR-α, reversed the reduction in the expression of PPAR-γ, PGC-1α, AMPK, GLUT4, Nrf2, p-eNOS, SOD, and CAT, and decreased the expression of Keap1, p47phox and NOX4. Therefore, the treatment with the H₂S donor protects cardiomyocytes from damage caused by hyperglycemia, HR, or both conditions by reducing oxidative stress markers and improving antioxidant mechanisms, thereby increasing cell viability and “cardiomyocyte ultrastructure”. Full article

This study applied K-means cluster analysis to urinary biomarker profiles in interstitial cystitis/bladder pain syndrome (IC/BPS) patients, aiming to provide a new perspective on disease classification and its clinical relevance. We retrospectively analyzed urine samples from 127 IC/BPS patients and 30 controls. The urinary levels of 10 inflammatory cytokines and three oxidative stress markers (8-hydroxy-2-deoxyguanosin [8-OHdG], 8-isoprostane, and total antioxidant capacity [TAC]) were quantified. K-means clustering was performed to identify biomarker-based patient subgroups. IC/BPS patients exhibited significantly elevated urinary levels of Eotaxin, MCP-1, NGF, 8-OHdG, 8-isoprostane, and TAC compared to controls (all p < 0.05). K-means clustering identified four distinct subgroups. Cluster 4, characterized by the highest levels of inflammatory and oxidative stress biomarkers, comprised 85% ESSIC type 2 IC/BPS patients and exhibited the lowest visual analogue scale (VAS) pain scores and maximal bladder capacity (MBC). Correlation analysis revealed distinct cluster-specific associations between biomarker levels and clinical parameters, including the VAS pain score, MBC, the grade of glomerulation, and treatment outcomes. Applying K-means clustering to urinary inflammatory and oxidative stress biomarkers provides a new perspective on disease classification, identifying IC/BPS subtypes with distinct clinical and biochemical characteristics. This approach may refine disease phenotyping and guide personalized treatment strategies in the future. Full article

Coking activities produce high concentrations of aromatic compounds (ACs) and related substances, which may have impacts on human health. However, the health effects of these substances on humans exposed to coking sites have not been fully elucidated. A total of 637 people were recruited to participate in this cross-sectional study. Using multiple linear regression and Bayesian kernel machine regression, we investigated the relationships between the urinary parent or metabolite forms of ACs (including metabolites of PAHs and their derivatives, nitrophenols, and chlorophenols) and hepatorenal biomarkers (HRBs), including total bilirubin, aspartate aminotransferase/alanine aminotransferase, serum uric acid, creatinine, albumin/globulin, and urea. The HRBs adopted in this study can effectively represent the status of human liver and kidney function. Mediation analysis was performed to investigate the possible mediating relationship between ACs and HRBs using oxidative stress markers as mediators. Our study indicated that ACs were significantly associated with increases in TBIL, AST/ALT, A/G, and UA, as well as a significant decrease in Cr. UREA showed no association with ACs among coking workers. The oxidative stress markers 8-hydroxy-2’-deoxyguanosine, 8-iso-prostaglandin-F2α, and 8-iso,15(R)-prostaglandinF2α mediated the induction of ACs on TBIL. Our results suggest that AC exposure in coking workers may be associated with adverse changes in hepatorenal biomarkers. This study highlights the significant impact of ACs from coking activities on workers’ hepatorenal biomarkers, providing crucial evidence for health risk assessment and prevention in affected populations. Full article

Research undertaken over the past few years has brought attention to the role of oxidative stress in the development of neoplasms by damaging nucleic acids, lipids, and proteins, thereby altering their normal function. In general, the levels of antioxidant enzymes are low in patients with neoplasms, and the biomarkers used to quantify oxidative stress have increased levels. Elevated levels of 8-hydroxy-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), as well as decreased levels of antioxidant enzymes, have been observed in patients diagnosed with colorectal cancer (CRC) at various stages of evolution, but further research is needed on the correlation between these biomarkers and disease progression. Inflammation enhances the production of reactive oxygen species and plays an important role in CRC development. Studies in the field of metabolomics have suggested that changes in serum metabolites might be indicators of the progression from adenoma to colorectal carcinoma, particularly those resulting from lipid metabolism. The role of lipidomics in the pathogenesis of CRC warrants further investigation, as these combinations of metabolites (metabolic fingerprints) may have the potential to become clinically useful markers. In this article, we review our current understanding of the interplay between oxidative stress, inflammatory markers and lipidomic products in the pathogenesis of CRC. Full article

Diabetes is associated with an increased risk of thromboembolism. However, the effects of apixaban, a factor Xa inhibitor on diabetic nephropathy, remain unknown. Six-week-old Wistar rats received a single 60 mg/kg intraperitoneal injection of streptozotocin to produce a model of type 1 diabetes. Type 1 diabetic and non-diabetic control rats were treated with or without apixaban orally for 8 weeks, and blood and kidneys were obtained for biochemical, real-time reverse transcription-polymerase chain reaction (RT-PCR) and morphological analyses. Although apixaban treatment did not affect glycemic or lipid parameters, it significantly (p < 0.01) inhibited the increases in advanced glycation end products (AGEs), the receptor for AGEs (RAGE) mRNA and protein levels, 8-hydroxy-2′-deoxyguanosine (8-OHdG), and NADPH oxidase-driven superoxide generation in diabetic rats at 14 weeks old. Compared with non-diabetic rats, gene and protein expression levels of monocyte chemoattractant protein-1 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF), and fibronectin were increased in 14-week-old diabetic rats, which were associated with enhanced renal expression of kidney injury molecule-1 (KIM-1) and Mac-3, increased extracellular matrix accumulation in the kidneys, and elevated urinary excretion levels of protein and KIM-1, all of which were significantly inhibited by the treatment with apixaban. Urine KIM-1 levels were significantly (p < 0.01) and positively correlated with AGEs (r = 0.690) and 8-OHdG (r = 0.793) in the kidneys and serum 8-OHdG levels (r = 0.823). Our present findings suggest that apixaban could ameliorate renal injury in streptozotocin-induced type 1 diabetic rats partly by blocking the AGE-RAGE-oxidative stress axis in diabetic kidneys. Full article

Background/Objectives: Inhalation of environmental particulate air pollution has been reported to cause pulmonary and systemic events including coagulation disturbances, systemic inflammation, and oxidative stress. Nerolidol, a naturally occurring sesquiterpene alcohol, has effective antioxidant and anti-inflammatory effects. Hence, the aim in the present investigation was to evaluate the potential ameliorative effects of nerolidol on the coagulation and systemic actions induced by pulmonary exposure to diesel exhaust particles (DEPs). Methods: Nerolidol (100 mg/kg) was given to mice by oral gavage one hour before the intratracheal instillation of DEPs (0.5 mg/kg), and 24 h later various markers of coagulation and systemic toxicity were evaluated. Results: Nerolidol treatment significantly abrogated DEP-induced platelet aggregation in vivo and in vitro. Nerolidol has also prevented the shortening of the prothrombin time and activated plasma thromboplastin time triggered by DEP exposure. Likewise, while the concentrations of fibrinogen and plasminogen activator inhibitor-1 were increased by DEP administration, that of tissue plasminogen activator was significantly decreased. These effects were abolished in the group of mice concomitantly treated with nerolidol and DEP. Moreover, plasma markers of inflammation, oxidative stress, and endothelial dysfunction which were significantly increased in the DEP-treated group, returned to control levels in the nerolidol + DEP group. Nerolidol treatment significantly ameliorated the increase in the concentrations of hypoxia-inducible factor 1α, galectin-3, and neutrophil gelatinase-associated lipocalin induced by pulmonary exposure to DEP. The co-administration of nerolidol + DEPs significantly mitigated the increase in markers of oxidative DNA damage, 8-hydroxy-2-deoxyguanosine, and apoptosis, cleaved-caspase-3, induced by DEP. Conclusions: Collectively, our data demonstrate that nerolidol exert significant ameliorative actions against DEP-induced thrombotic events, endothelial dysfunction, systemic inflammation, oxidative stress, DNA damage, and apoptosis. Pending further pharmacological and toxicological studies, nerolidol could be a promising agent to alleviate the toxicity of inhaled DEPs and other pollutant particles. Full article

Non-alcoholic fatty liver disease (NAFLD) is a global cause of liver dysfunction. This spectrum of hepatic disorders can progress to severe conditions, such as non-alcoholic steatohepatitis (NASH) and cirrhosis, due to oxidative stress and sustained cellular injury. With limited pharmacological options, glutathione (GSH), a key antioxidant, has shown promising potential in reducing oxidative stress, maintaining redox balance, and improving liver function. This literature review examines studies from 2014–2024 exploring GSH therapy in NAFLD patients. Eligible studies assessed GSH as the primary intervention for NAFLD in human subjects, reporting outcomes such as liver function or oxidative stress markers. Randomized clinical trials (RCTs) were eligible, while combination therapy studies were included if GSH’s effect could be isolated. Exclusions applied to non-NAFLD studies, animal/in vitro models, and non-GSH antioxidant interventions. Analysis of three studies (totaling 109 participants) demonstrated consistent improvements in alanine transaminase (ALT) levels and reductions in oxidative stress markers like 8-hydroxy-2-deoxyguanosine (8-OHdG). However, small sample sizes and inconsistent protocols limit generalizability. Further large-scale RCTs are required to confirm GSH’s efficacy, determine optimal dosing, and assess long-term effects. This literature review highlights GSH’s potential as a novel NAFLD therapeutic strategy while emphasizing the need for further studies to refine its clinical application. Full article

Purpose: Interstitial cystitis/bladder pain syndrome (IC/BPS) is mysterious and difficult to diagnose without cystoscopic hydrodistention. This study aimed to explore non-invasive and highly reliable urine biomarkers to identify Hunner’s IC (HIC) and different non-Hunner’s IC (NHIC) subtypes. Methods: In total, 422 women with and without clinically diagnosed IC/BPS (n = 376 and 46, respectively) were retrospectively enrolled. Patients were diagnosed with HIC or NHIC by cystoscopic hydrodistention under anesthesia. Then, the maximal bladder capacity (MBC) and glomerulation grade were determined. Thirteen urine inflammatory cytokines, chemokines, and oxidative stress biomarkers based on the previously reported predictors of IC/BPS were assayed using commercial microsphere kits. The dataset was randomly divided into training (70%) and test (30%) sets for model construction and validation using logistic regression and stepwise variable selection techniques. To construct the predictive models, univariate analysis was performed to evaluate the discriminative power of each urinary biomarker, measured by the area under the curve (AUC). Biomarkers with AUC values < 0.6 were excluded from further modeling. Multivariate logistic regression was then employed, with variables selected through stepwise forward selection based on log-likelihood criteria. For dichotomization, cutoff values were determined using quartile ranges from the control group. The final model’s performance was assessed using AUC, accuracy, sensitivity, and specificity in both training and test sets. Results: By setting the screening criterion to AUC ≥ 0.60, the potential urinary biomarkers for identifying IC/BPS cases were eotaxin, monocyte chemoattractant protein-1, tumor necrosis factor-alpha (TNF-α), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and 8-isoprostane. Those for identifying HIC from the IC/BPS cohort were interleukin (IL)-6, IL-8, interferon γ-inducible protein 10 (IP-10), and regulated on activation, normal T-cell expressed and secreted (RANTES). A diagnostic algorithm using a cluster of urinary biomarkers included TNF-α ≥ 0.95 pg/mL or 8-OHDG ≥ 22.34 pg/mL and 8-isoprastane ≥ 22.34 pg/mL for identifying IC/BPS from the overall cohort; for identifying HIC from the IC/BPS cohort, the urinary IP-10 ≥ 3.74 pg/mL or IP-10 ≥ 19.94 pg/mL was added. Conclusions: Using a cluster of urinary biomarkers such as TNF-α or 8-OHdG and 8-isoprostane can identify IC/BPS from a study cohort, and adding the urinary IP-10 can distinguish HIC from IC/BPS cases. Full article