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Background: This study investigated the effects of Laurocerasus officinalis Roem (cherry laurel; CL), a traditionally consumed fruit, on cognitive performance and selected neurobiochemical and metabolic pathways in a nontransgenic streptozotocin (STZ)-induced Alzheimer’s disease (i.c.v. STZ) model and an STZ-induced type 2 diabetes mellitus (T2DM; i.p. STZ) model. Method: Fifty-seven adult male Sprague–Dawley rats were allocated to control, T2DM, and Alzheimer (ALZ) model groups, with subgroup interventions including CL supplementation and, in the T2DM model, metformin as a comparator. Spatial learning and memory were assessed using the Morris Water Maze. Serum and brain tissue levels of GSK3-β, glutathione (GSH), interleukin-1 (IL-1), GLUT4, GLP-1, β-amyloid (Aβ), and acetylcholinesterase (AChE) were quantified. Results: Serum GSK3-β levels did not differ significantly between groups, whereas brain tissue GSK3-β showed significant between-group differences. CL increased GSH levels in both models, with significant elevations in serum and brain tissue GSH in the ALZ model following CL administration; in the T2DM model, GSH increased after both CL and metformin. In the ALZ model, CL was associated with decreased serum Aβ and AChE levels and improved Morris Water Maze performance, reflected by reduced escape latencies. Conclusions: CL supplementation was associated with antioxidant enhancement and modulation of amyloid- and cholinergic-related measures, alongside improved spatial learning performance in the STZ-induced nontransgenic ALZ model. In addition, CL reduced blood glucose in the T2DM model. Given the likely contribution of fruit phytochemicals (including total phenolics), further studies are warranted to better define the bioactive composition and mechanisms underlying these effects.

Proteinopathies are characterized by aging related accumulation of misfolded protein aggregates. Irreversible covalent modifications of aging proteins may significantly affect the native three dimentional conformation of proteins, alter their function and lead to accumulation of misfolded protein as dysfunctional aggregates. Protein misfolding and accumulation of aberrant proteins are known to be associated with aging-induced proteinopathies such as amyloid ß and tau proteins in Alzheimer’s disease, α-synuclein in Parkinson’s disease and islet amyloid polypeptides in Type 2 diabetes mellitus. Protein oxidation processes such as S-nitrosylation, dityrosine formation and some of the newly elucidated processes such as carbamylation and citrullination recently drew the attention of researchers in the field of Gerontology. Studying over these processes and illuminating their relations between proteinopathies may help to diagnose early and even to treat age related disorders. Therefore, we have chosen to concentrate on aging-induced proteinopathic nature of these novel protein modifications in this review.

Background Saliva contains a variety of biochemical compounds, including antioxidants, and serves as the body’s first line of defense against oxidative stress caused by free radicals. The aim of this study was to investigate the effects of dental treatments on salivary oxidative stress biomarkers in children aged 3–5 years with severe early childhood caries (S-ECC) compared to children without caries. Method This study was conducted on 20 children aged 3–5 years with severe early childhood caries (S-ECC) and 20 children without caries. Salivary oxidative stress biomarkers and antioxidants were measured after the initial examination (T0), after the end of restorative treatments (T1), and after fluoride varnish applications (T2). Post hoc Bonferroni test was used to compare normally distributed parameters between T0-T1-T2 times. Pearson correlation analysis was used to examine the relationships between parameters that conform to normal distribution. The Mann-Whitney U test was used to compare the parameters in the control and experimental groups. Significance was evaluated at the  p  < 0.05 level. Results The mean dmft of the participants in the study group was 8.86 ± 14.5. Advanced oxidation protein products (AOPP), dityrosine (DT), kynurenine (KYN), advanced glycation end products (AGE), lipid hydroperoxides (LHP) and malondialdehyde (MDA) values decrease after the treatment of dental caries and protective fluoride varnish applications, while an increases in total thiol (TSH) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) values were observed after protective varnish applications compared to pre-treatment values. Antioxidant parameters at time T2 in the study group were statistically significantly higher than in the control group ( p  < 0.05). In the study group, there was no correlation between TSH and oxidative stress mediators in terms of changes at time T1 post-treatment compared to the pre-treatment period, while an inverse moderate relationship was found with AGE and LHP in terms of changes at time T2 post-treatment ( p  < 0.05). Conclusions An increase in salivary antioxidants was detected after dental restorations were completed and protective fluoride varnish application, while a decrease in oxidative stress markers was detected. Clinical relevance Fluoride varnish applications applied in the study group may further reduce the oral microbiome load and cause salivary oxidative stress markers to be significantly lower than in the control group.

Myocardial infarction (MI) is defined as a clinical event in which myocardial damage is evidenced in the setting of myocardial ischemia. However, patients without occlusive coronary artery stenosis can also have myocardial infarction, which is titled Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA). In our study, we aimed to evaluate oxidative stress and inflammation responses between MINOCA and MI with coronary artery disease (CAD) patients. In this prospective, cross-sectional study, patients with elevated cardiac markers who were admitted to the cardiology clinic between March 2024 and May 2024 with the preliminary diagnosis of acute coronary syndrome were included. Patients were consecutively collected as those with an occlusive lesion on coronary angiography and those without. Routine blood samples and oxidative stress parameters were obtained and compared between groups. A total of 88 patients, including 44 MINOCA and 44 MI-CAD patients, were included in the study. The MINOCA group was significantly younger than the MI-CAD group (56.2 ± 12.5, vs. 64.7 ± 9.3, p: 0.001). While inflammatory parameters were similar between groups, dityrosine (5708 FU/mL (5311–6417) vs. 4488 FU/mL (3641–5238), p < 0.001), lipid hydroperoxide (3.6 nmol/mL (3.4–3.9) vs. 3.4 nmol/mL (3.1–3.9), p: 0.023), kynurenine (3814 ± 621 FU/mL vs. 3319 ± 680 FU/mL, p: 0.001), and malondialdehyde (17.4 nmol/mL (13.7–19.1) vs. 13.1 nmol/mL (12–14.9), p < 0.001) levels were higher in the MI-CAD group than in the MINOCA group. Although inflammation parameters did not differ between MI-CAD and MINOCA patients, oxidative stress parameters were higher in the MI-CAD group. Regardless of the presence and severity of inflammation, oxidative markers can help to assess the level of myocardial cell damage, risk stratification, and diagnosis of myocardial infarction.

ABSTRACT Background: Intercellular adhesion molecule-1 (ICAM-1) is a surface glycoprotein important for tumor invasion and angiogenesis. The present research is conducted to investigate whether specific gene polymorphism of ICAM-1 K469E (rs5498) and plasma redox status could be associated with laryngeal cancer (LC) development. Since there is no clear evidence which investigates the relationship between ICAM-1 polymorphism and ROS-mediated plasma protein oxidation in LC, our study is the first significant contribution for investigating the relationship. Methods: The study covered patients with primary LC and their age-matched healthy control subjects. Evaluation of ICAM-1 K469E (rs5498) gene polymorphism was performed by polymerase chain reaction-restriction fragment length polymorphism. Plasma redox status was assessed with spectrophotometric methods. Results: In the current paper, we found that LC patients with GG genotype had a decreasing trend for the plasma oxidative damage biomarker levels when compared with all allele genotypes (AA and AG). Conclusion: We concluded that G allele of the ICAM-1 K469E gene plays a significant role in the optimal regulation of plasma redox homeostasis in patients with LC.

Laryngeal tumours with multifactorial etiopathogenesis constitute ∼1% of all body cancers. The imbalance between oxidative and antioxidative systems affects redox-homeostasis. The oxidative stress generated by the continuous formation of reactive oxygen species results in the oxidation of cellular molecules. The present study investigated the protein oxidation levels and the distribution of receptors for advanced glycation end products (RAGE) variants in the risk of laryngeal carcinoma (LC). RAGE gene polymorphisms were determined by restriction endonuclease-based assay in 120 controls and 120 LC patients. Spectrophotometric methods were used to determine oxidant and antioxidant parameters including protein-carbonyl-groups (PCO), advanced-oxidation-protein-products (AOPP), lipid-hydroperoxides (LPH), thiol-fractures, superoxide-dismutase (SOD) activity. The distributions of rs1800624 and rs2070600 genotypes differed non-significantly among the study groups, however, the rs2070600-Ser allele had a higher frequency among the patients. While rs1800624-A allele carriers had higher frequency of perineural and lymphatic invasion, rs2070600-Ser allele frequency was higher in advanced-stage patients and in patients with muscle and perineural invasion. PCO, AOPP, LPH levels, and SOD activity were significantly higher in the patients. According to AUCs all of them are of diagnostic importance, therefore, cut-off values were determined. The analysis of the combined effects of RAGE polymorphisms and the oxidative stress parameters showed that LPH, thiols, and SOD activity differ among RAGE variants. Our results suggest that high levels of serum PCO, AOPP, LPH, and SOD activity and rs2070600-Ser allele may have effects on LC risk individually and both polymorphisms of RAGE may affect the progression of the disease by interacting with the oxidant-antioxidant system.

Aging is characterized by a gradual functional decrease of all systems including the kidneys. Growing evidence links altered lipid protein redox-homeostasis with renal dysfunction. The effect of sexual dimorphism on the lipid protein redox-homeostasis mechanisms in the aging kidney is obscure. In the current study, we aimed to investigate redox homeostasis as it related to sexual dimorphism on protein oxidation and lipid peroxidation parameters, as protein carbonyl (PCO), total thiol (T-SH), advanced oxidation protein products (AOPP), malondialdehyde, glutathione (GSH), and superoxide dismutase (SOD) activity, as potential aging biomarkers, which may contribute to an analysis of the free radical theory of aging. The study was carried out with 16 naturally aged rats (24 months old; eight males and eight females) and their corresponding young rat groups as controls (6 months old; eight males and eight females). All of the aforementioned parameters (PCO, T-SH, AOPP, MDA, GSH, SOD) were measured manually instead of automated devices or ELISA kits. PCO, AOPP, and malondialdehyde levels in aged rats were significantly higher in the older rat group than in the younger rat group, whereas SOD activities were significantly lower in old rats. T-SH levels were not significantly different in male groups; however, T-SH levels were lower in the aged female group than in the young female control group. In addition, GSH levels were significantly different between the aged rat group and the corresponding young control group for both genders. With respect to PCO and AOPP, impaired redox homeostasis is substantially more prominent in males than females. The decrease of G-SH levels in male groups could be attributed to stabilizing the redox status of protein thiol groups by the depletion of the GSH groups. Considering the results, the renal tissue proteins and lipids in different genders may have different susceptibilities to oxidative damage.

Metformin has been suggested to have protective effects on the central nervous system, but the mechanism is unknown. The similarity between the effects of metformin and the inhibition of glycogen synthase kinase (GSK)-3β suggests that metformin may inhibit GSK-3β. In addition, zinc is an important element that inhibits GSK-3β by phosphorylation. In this study, we investigated whether the effects of metformin on neuroprotection and neuronal survival were mediated by zinc-dependent inhibition of GSK-3β in rats with glutamate-induced neurotoxicity. Forty adult male rats were divided into 5 groups: control, glutamate, metformin + glutamate, zinc deficiency + glutamate, and zinc deficiency + metformin + glutamate. Zinc deficiency was induced with a zinc-poor pellet. Metformin was orally administered for 35 days. D-glutamic acid was intraperitoneally administered on the 35th day. On the 38th day, neurodegeneration was examined histopathologically, and the effects on neuronal protection and survival were evaluated via intracellular S-100β immunohistochemical staining. The findings were examined in relation to nonphosphorylated (active) GSK-3β levels and oxidative stress parameters in brain tissue and blood. Neurodegeneration was increased ( p  < 0.05) in rats fed a zinc-deficient diet. Active GSK-3β levels were increased in groups with neurodegeneration ( p  < 0.01). Decreased neurodegeneration, increased neuronal survival ( p  < 0.01), decreased active GSK-3β ( p  < 0.01) levels and oxidative stress parameters, and increased antioxidant parameters were observed in groups treated with metformin ( p  < 0.01). Metformin had fewer protective effects on rats fed a zinc-deficient diet. Metformin may exert neuroprotective effects and increase S-100β-mediated neuronal survival by zinc-dependent inhibition of GSK-3β during glutamate neurotoxicity.

BACKGROUND: Th is study evaluated the use of metformin or pioglitazone in preventing or reducing the development of postoperative intra-abdominal adhesion (PIAA) by employing histopathological, immunohistochemical, and biochemical analyses in an experimental adhesion model. METHODS: Fifty Wistar-Albino rats were divided into five groups: Group I (Control), Group II (Sham Treatment), Group III (Hyaluronic Acid), Group IV (Metformin), and Group V (Pioglitazone). Adhesions were induced in the experimental groups, except for the sham group, using the scraping method. After 10 days, rats were euthanized for evaluation. Macroscopic adhesion degrees were assessed using Nair's scoring system. Immunohistochemical and enzyme-linked immunosorbent assay (ELISA) methods were utilized to assess serum, peritoneal lavage, and intestinal tissue samples. Fructosamine, interleukin-6 (IL-6), transforming growth factor-beta (TGF-[beta]), and fibronectin levels were measured in serum and peritoneal lavage samples. RESULTS: The groups exhibited similar Nair scores and Type I or Type III Collagen staining scores (all, p>0.05). Pioglitazone significantly reduced serum IL-6 and TGF-[beta] levels compared to controls (p=0.002 and p=0.008, respectively). Both metformin and pioglitazone groups showed elevated IL-6 in peritoneal lavage relative to controls, while fibronectin levels in the lavage were lower in pioglitazone-treated rats compared to the sham group (all, p<0.005). CONCLUSION: Pioglitazone, but not metformin, demonstrated a positive biochemical impact on preventing PIAA formation in an experimental rat model, although histological impacts were not observed. Further experimental studies employing different dose/ duration regimens of pioglitazone are needed to enhance our understanding of its effect on PIAA formation. Keywords: Pioglitazone; adhesion; adhesion model; metformin; peroxisome proliferator-activated receptor (PPAR). AMAC: Siganlarda olusturulan deneysel bir adezyon modelinde histopatolojik, immunohistokimyasal ve biyokimyasal analizier kullanilarak postoperatif karin igi adezyon (PIAA) gelisimini onleme veya azaltmada metformin ve pioglitazonun etkisini degerlendirmek. GEREC VE YONTEM: Elli Wistar-Albino cinsi sigan bes gruba ayrildi: Grup I (kontrol), Grup II (sham), Grup III (Hyaluronik asit), Grup IV (metformin) ve Grup V (pioglitazon). Sham deney grubu disindaki tum deney gruplarinda yapisikliklar scraping model olusturularak yapildi ve 10 gun sonra degerlendirme igin siganlara otenazi uygulandi. Makroskopik adezyon dereceleri Nair skor sistemi kullanilarak degerlendirildi. Serum ve periton lavaj orneklerinde fruktozamin, IL-6, TGF-[beta] ve fibronektin duzeyleri olguldu. Bagirsak doku orneklerinin degerlendirilmesinde histopatolojik skorlama sistemi kullanildi ve immunohistokimyasal kitlerden yararlanildi. BULGULAR: Gruplar Nair skorlamasi ve Tip I–Tip III Kollajen boyanma skorlari agisindan benzerdi (hepsi, p>0,05). Pioglitazon grubunda kontrol grubuna kiyasla serum IL-6 ve TGF-p duzeylerini anlamli duzeyde dusuk saptandi (sirasiyla p=0,002 ve 0,008). Metformin ve pioglitazon gruplari peritoneal lavajda kontrol grubuna kiyasla daha yuksek IL-6 sergilerken, peritoneal lavajdaki fibronektin seviyeleri pioglitazon ile tedavi edilen siganlarda sham grubuyla karsilastirildiginda daha dusuk saptandi (hepsi, p<0.005). SONUC: Deneysel adezyon modelinde PIAA olusumunun onlenmesinde pioglitazon histolojik olarak olmasa da biyokimyasal olarak olumlu bir etkiye sahipti. PIAA olusumu uzerindeki etkisini daha iyi anlamak igin pioglitazonun farkli doz/sure rejimlerini kullanan ileri deneysel galismalara ihtiyag vardir. Anahtar sozcukler: Adezyon; adezyon model; metformin; pioglitazon; PPAR.

This study was aimed to assess oxidative stress, pro-inflammatory cytokines and some trace elements in healthy pet cats exposed to environmental tobacco smoke. Forty healthy cats were included in this study. Cats were divided in two groups: Exposed to tobacco smoke (ETS; n = 20) and non-exposed to tobacco smoke (NETS; n = 20). Blood levels of cotinine, total oxidant status (TOS), oxidative stress index (OSI), lipid hydroperoxide (LOOH), protein carbonyl (PCO), advanced oxidative protein products (AOPP), total antioxidant status (TAS), copper, zinc-superoxide dismutase (Cu, Zn-SOD), catalase (CAT), total thiol (T-SH), interferon gamma (INF-γ), tumor necrosis factor (TNF-α), interleukin β (IL-1β), interleukin 6 (IL-6), interleukin-8 (IL-8), inter-leukin 2 (IL-2) and iron (Fe), zinc (Zn), copper (Cu), selenium (Se) levels were measured. Hematological and biochemical parameters were also measured. Serum cotinine, TOS, OSI, PCO, AOPP and LOOH levels were higher, whereas TAS and Cu, Zn-SOD levels were lower in ETS group. In ETS group INF-γ, IL-1β, IL-2, and IL-6 levels were higher. The Cu level was higher in ETS group. Blood reticulocyte number, serum creatinine and glucose were higher in ETS group. It could be concluded that exposure to tobacco smoke in cats impaired the oxidant/antioxidant balance and potentially triggered the release of pro-inflammatory cytokines.