Bisphenol A (BPA) is a pervasive endocrine-disrupting chemical with documented toxic effects in living organisms. This study evaluated the protective potential of vanillic acid (VA) against BPA-induced toxicity in Drosophila melanogaster. BPA exposure elevated lipid peroxidation (MDA), reduced antioxidant defenses (SOD and CAT activities and GSH content), increased DNA damage (Comet assay), lowered acetylcholinesterase levels, and impaired developmental parameters (pupation, climbing, crawling, lifespan, and food intake). BPA also upregulated SOD, CAT, gclc, hsp70, CncC, and Keap1 mRNA expression, indicating activation of the cellular stress response. VA co-treatment dose-dependently mitigated these effects, restoring redox balance, reducing DNA strand breaks at the highest VA dose, and rescuing developmental endpoints. These findings suggest that VA is an effective natural protective agent against BPA toxicity in vivo, an effect accompanied by modulation of CncC/Keap1 pathway gene expression.

Syringaldehyde (SG) is a naturally derived phenolic aldehyde known for a range of biological activities. This study evaluated its protective potential against the chemically induced gastric injury model and investigated the underlying mechanisms involved. Acute gastric ulceration was induced in male Swiss albino mice by intragastric administration of a mixture of 0.3 M HCl and 70

Exposure to certain pesticides remains a significant environmental and public health concern due to their capacity to induce oxidative damage in vital organs. Deltamethrin (DEL), a widely used synthetic pyrethroid, disrupts hepatic function primarily through oxidative stress-mediated mechanisms. This study investigated the protective effects of spinosin (SP) and carvacrol (CAR), administered individually or in combination, against DEL-induced liver toxicity and explored the underlying molecular pathways. Hepatic injury was induced in male Swiss albino mice by oral gavage of DEL (15 mg/kg bw). SP and CAR were administered at 50 mg/kg bw, either alone or in combination, while silymarin (50 mg/kg bw) served as a reference compound. All treatments were administered once daily for 28 consecutive days. DEL exposure significantly reduced SOD, CAT, GSH, and PGE2 levels, accompanied by downregulation of HO-1, Nrf2, and Bcl-2 expression. Conversely, levels of ALP, ALT, AST, MDA, NO, TNF-α, IL-1β, IL-6, Bax, and Cas-3 were significantly increased. Treatment with SP and CAR ameliorated these alterations, with combined administration demonstrating greater efficacy than monotherapy. Overall, the findings suggest that SP and CAR co-treatment may exert enhanced hepatoprotective effects, potentially through coordinated regulation of oxidative stress, inflammation, apoptosis, and activation of the Nrf2/HO-1 signaling pathway.

Antibiotic residues in water buffalo milk are a food-safety concern, yet depletion data are scarce. The purpose of this study was to characterize the depletion profiles of amoxicillin (AMOX) and its two major metabolites, amoxicilloic acid (AMA) and amoxicillin diketopiperazine-2',5'-dione (2,5-DKP), in Anatolian water buffalo milk after a single intramuscular administration and to estimate a milk withdrawal time relative to the EU MRL. We tested the hypothesis that AMOX concentrations would decrease below the EU MRL over successive milkings and that AMA and 2,5-DKP would exhibit depletion kinetics distinct from the parent compound. Five lactating Anatolian water buffaloes received a single intramuscular injection of amoxicillin (15 milligrams per kilogram). Milk was collected at each milking (twice daily) for seven days and analyzed by liquid chromatography-tandem mass spectrometry with quantification limits below the European Union maximum residue limit for amoxicillin in milk (4 micrograms per kilogram). Amoxicillin peaked at the second milking (mean 13.65 micrograms per kilogram), mean concentrations fell below the maximum residue limit from the sixth milking, and they became non-quantifiable from the tenth milking onward. Two major metabolites, amoxicillinic acid and amoxicillin diketopiperazine-2',5'-dione, peaked earlier (2,5-DKP Tmax 12 h) or at higher concentrations (AMA Cmax 32.64 µg/kg vs. AMOX 13.65 µg/kg) and remained detectable up to the thirteenth milking, with longer apparent terminal half-lives (32.0 and 52.8 h) than amoxicillin (23.5 h); the mixed-effects model confirmed different depletion rates among analytes (milking × analyte interaction p = 4.63 × 10-5). A log-linear withdrawal model applying the EMA 95/95 tolerance limit indicated that the first time point at which the upper tolerance limit fell below the EU MRL was 84.7 h after dosing; rounded up to the next 12 h milking interval, this corresponds to a reported withdrawal period of 96 h (≈8 milkings). These results provide species-specific residue kinetics for amoxicillin in Anatolian buffalo milk and support considering metabolites in monitoring and withdrawal-time decisions.

Exposure to pesticides poses a substantial global public health challenge. Among these agents, deltamethrin (DEL), a commonly applied synthetic pyrethroid in agricultural practices, has attracted particular concern due to its bioaccumulative potential and its capacity to induce cellular injury via oxidative stress mechanisms, with the liver being especially vulnerable. Syringaldehyde (SYR) is a naturally derived polyphenolic compound within the flavonoid class and has been reported to exhibit therapeutic properties in various pathological conditions. The current investigation was designed to evaluate the hepatoprotective efficacy of SYR and to clarify the underlying mechanisms involved in DEL-induced hepatic damage. Experimental hepatotoxicity was established in mice by intragastric administration of DEL (15 mg/kg). SYR was administered orally at doses of 25 and 50 mg/kg, while silymarin (50 mg/kg) served as a reference hepatoprotective agent. DEL exposure produced marked elevations in serum liver enzymes (AST, ALT, and ALP), lipid peroxidation indices (MDA), nitric oxide levels, pro-inflammatory mediators (NFκB, iNOS, Cox-2, TNF-α, IL-1β, and IL-6), and pro-apoptotic proteins (Bax and Cas-3). Concurrently, significant reductions were observed in GSH, SOD, and CAT, PGE2, and the expression of cytoprotective and anti-apoptotic markers, including Nrf2, HO-1, and Bcl-2. In comparison with the DEL-treated group, SYR supplementation markedly mitigated hepatic enzyme leakage, inflammatory and oxidative stress markers, and apoptotic protein expression, while restoring antioxidant capacity, PGE2 levels, and the expression of Nrf2, HO-1, and Bcl-2. Collectively, these findings provide strong evidence that SYR confers protection against DEL-induced liver injury in mice, primarily through modulation of the Nrf2/HO-1 signaling pathway.

Acrylamide, a chemical used in industrial applications, has been classified as an environmental toxin owing to its widespread contamination of drinking water and groundwater resources. Vanillic acid (VA) is a phenolic compound naturally occurring in numerous dietary sources and medicinal plants. VA exhibits a wide range of pharmacological properties, including antioxidant, anti-inflammatory, and neuroprotective activities. This study investigated the protective effects of VA against acrylamide-induced oxidative stress in Drosophila melanogaster at developmental, biochemical, and molecular levels. D. melanogaster were exposed to acrylamide (2 mM) alone or with VA at three doses (0.1, 0.5, and 1 mg/L). Acrylamide exposure elevated reactive oxygen species and lipid peroxidation, decreased antioxidant enzyme activities (SOD, CAT) and glutathione (GSH) levels, increased DNA damage by the Comet assay, upregulated mRNA expression of stress-related genes (SOD, CAT, gclc and hsp70) and detoxification-pathway components (Keap1 and CncC/Nrf2), and adversely affected developmental parameters (larval toxicity, crawling, climbing, survival, food intake, body weight and length). Co-administration of VA dose-dependently reduced lipid peroxidation and ameliorated antioxidant enzyme activities and DNA damage. VA also modulated the impaired developmental parameters of acrylamide-exposed larvae. These findings indicate that VA possesses considerable protective potential against acrylamide toxicity, with important implications for environmental and human health.

Cisplatin (CIS) is a highly effective chemotherapeutic drug, but one of its most serious side effects is hepatonephrotoxicity, which varies based on its dosage and duration of use. Previous studies have reported that obtusifolin (OBS) exhibits several pharmacological effects, including antioxidant and antidiabetic activities. In this study, we investigated the protective effects of OBS against CIS-induced hepatonephrotoxicity. OBS (0.5 and 1 mg/kg, i.p.) was administered to male mice for 10 days, while CIS (20 mg/kg, i.p.) was administered on day 7 to induce hepatonephrotoxicity. The results showed that OBS reduced the CIS-induced elevations in AST, ALT, ALP, BUN, and creatinine levels by approximately 14

Metaflumizone (MTF) is a pyrazoline sodium channel blocker (SBI) insecticide, and data on its toxicity are limited. Taurine (2-aminoethanesulfonic acid) is a sulfur-containing β-amino acid that is naturally found in high concentrations in cells. In this study, we thoroughly evaluated the impact of taurine on MTF-induced hepatonephrotoxicity in a rat model, focusing on oxidative stress, inflammatory responses, and programmed cell death. In the present study, MTF (500 mg/kg, orally) to induce hepatonephrotoxicity was delivered to male rats for 30 days, and taurine at different concentrations (50, 100, and 200 mg/kg, orally) was used for protective effect for the same period. Taurine treatment alleviated the elevated levels of AST, ALT, ALP, BUN, and creatinine caused by MTF. It further suppressed malate dehydrogenase levels and enhanced antioxidant defense by elevating SOD, GSH, and CAT levels. Additionally, taurine increased the mRNA expression levels of Bcl-2, which had been reduced due to oxidative stress, inflammatory, and apoptotic pathways, while suppressing the elevated gene expression levels of NFκB, TNF-α, Bax, and Cas-3. Furthermore, taurine regulated the altered protein expression levels of Bcl-2, Bax, and TNF-α induced by MTF. Microscopically, taurine also mitigated liver and kidney tissue damage caused by MTF. In conclusion, taurine significantly reduced MTF-induced hepatonephrotoxicity by suppressing oxidative stress, inflammatory responses, and programmed cell death. These findings indicate that taurine has the potential to be a treatment option in the case of the prevention of liver and kidney damage caused by SBI.

Paracetamol (Para) is a commonly employed nonsteroidal anti-inflammatory agent recognized for its potent analgesic and antipyretic effects; nevertheless, its use is often associated with severe hepatonephrotoxic side effects. Alizarin (ALZ), an anthraquinone compound, demonstrates antiproliferative and strong radical-scavenging properties. However, it remains unknown whether ALZ has any effects on hepatonephrotoxicity caused by the use of these drugs. This study investigated how ALZ modulates Paracetamol-induced liver and kidney toxicity in mice, with particular emphasis on the induction of the Nrf2/HO-1 regulatory pathway. For this purpose, ALZ (25 and 50 mg/kg, p.o.) and Para (250 mg/kg, p.o.) were applied to male mice for a duration of 14 days to induce hepatonephrotoxicity. ALZ administration alleviated the elevated biochemical indicators (ALT, AST, BUN, ALP, and creatinine) caused by Para. Additionally, ALZ reduced lipid peroxidation by decreasing MDA levels in tissues and improved antioxidant levels by increasing GSH, SOD, and CAT levels. Moreover, ALZ enhanced the mRNA expression levels of HO-1, Nrf2, and Bcl-2, which had been reduced by inflammation, oxidative stress, and apoptotic processes, while suppressing the increased gene expression levels of Bax, NFκB, Cas-3, and TNF-α. Furthermore, ALZ regulated the protein expression levels of Bax, Nrf2, Bcl-2, and Cas-3, which were altered by Para administration. Histopathological evaluations revealed that ALZ alleviated the tissue injuries in the liver and kidneys induced by Paracetamol. Overall, ALZ demonstrated a protective effect against Para-related hepatonephrotoxicity by attenuating oxidative stress, inflammatory responses, and apoptotic activity through Upregulation of the Nrf2/HO-1 signaling cascade. These results indicate that ALZ has potential therapeutic effects against liver and kidney damage.

In the present study, we investigated the protective effects of spinosin (SP) against cyclophosphamide (CYC)-induced hepatorenal toxicity in a mouse model. Fifty-six animals were randomly divided into eight groups. The control group received an intraperitoneal (i.p.) injection of 0.1 mL physiological saline, whereas the dimethyl sulfoxide (DMSO) group was given 0.1 mL of 1% DMSO orally. The CYC group was administered with 30 mg/kg CYC (i.p.) dissolved in physiological saline, while the SP group received 20 mg/kg SP orally dissolved in DMSO. The SP + CYC combination groups received SP orally at doses of 5, 10, or 20 mg/kg together with 30 mg/kg CYC (i.p.). Additionally, the silymarin (SLY) + CYC group received 50 mg/kg SLY orally and 30 mg/kg CYC (i.p.). The experimental protocol lasted for 10 days. SP treatment alleviated the CYC-induced elevations in plasma AST, ALT, BUN, and creatinine levels. It further suppressed lipid peroxidation by lowering MDA levels and enhanced antioxidant defense by increasing GSH levels and SOD and CAT activities in the liver and kidney. Additionally, SP increased the mRNA expression levels of HO-1, Nrf2, and Bcl-2 while suppressing the elevated expression of NFκB, TNF-α, Bax, and Caspase-3. Furthermore, SP normalized the altered protein expression levels of TNF-α, Caspase-3, and Bax induced by CYC. Histopathological analysis revealed that SP also ameliorated CYC-induced liver and kidney tissue damage. In conclusion, SP markedly attenuated CYC-induced hepatorenal toxicity by inhibiting oxidative stress, inflammation, and apoptosis. These results suggest that SP may represent a promising candidate for preventing liver and kidney injury associated with chemotherapeutic agents.

Alpha-amylase is an extracellular enzyme abundantly produced from fungal sources. The catalytic activity of microbial enzymes is higher, more stable, and economical compared to plant and animal enzymes; they can be produced in large quantities in a short time and do not produce unwanted by-products. In this study, the genotoxic effect of different concentrations (25 mg/mL, 50 mg/mL, and 100 mg/mL) of a native fungal thermostable alpha-amylase enzyme, produced from the Aspergillus niger G2-1 isolate with an enzyme activity of 38.6 U/mg, was investigated on the Drosophila melanogaster model organism. The effect of the alpha-amylase enzyme added to the culture medium on the developmental performance of D. melanogaster was assessed through larval toxicity analysis, its effect on DNA damage through the comet assay, and its response to oxidative stress through various biochemical parameters. As a result, it was determined that low-dose alpha-amylase enzyme concentration (25 mg/mL) did not cause intracellular oxidative stress, did not cause genotoxicity, and did not adversely affect growth performance, although feeding with alpha-amylase at 50 mg/mL and 100 mg/mL concentrations caused a significant decrease in the survival rate of D. melanogaster larvae and an increase in DNA damage rate in imagos. However, oxidative stress parameters in adult D. melanogaster did not change after the same alpha-amylase application.

Bal Ömer Çakmak, Muhsin Öztürk Propolis Azim Şimşek, Halil Yalçın Polen Fahriye Kan, İsmail Küçükkurt Arı Ekmeği (Perga) Fahriye Kan, Sinan İnce, Fatih Ramazan İstanbullugil Bal Mumu Ömer Çakmak, Muhsin Öztürk Arı Sütü ve Apilarnil Ali Soylu, Damla Arslan Acaröz, Zeki Gürler Arı Zehri Tuncer Çakmak Ulaş Acaröz Yakup Can Sancak

ABSTRACT Cyclophosphamide (CYC) is one of the most potent antineoplastic drugs; however, hepatonephrotoxicity, observed following its use, remains one of its most severe side effects. Previous studies have reported that syringaldehyde (SYA), a flavonoid compound, exhibits anti‐inflammatory and antioxidant properties. However, it is unclear whether SYA has any effects on hepatonephrotoxicity caused by the side effects of antineoplastic drugs. In the present research, we thoroughly evaluated the effects of SYA on cyclophosphamide‐induced hepatonephrotoxicity in a mouse model, focusing on Nrf2/HO‐1 pathway activation. In the present study, SYA (25 and 50 mg/kg, p.o.) and CYC (30 mg/kg, i.p.) were delivered to male mice for 10 days to induce hepatonephrotoxicity. SYA treatment alleviated the elevated levels of AST, ALT, BUN, and creatinine caused by CYC. It further suppressed lipid peroxidation by lowering MDA levels and enhanced antioxidant defense by elevating GSH, SOD, and CAT levels. Additionally, SYA increased the mRNA expression levels of HO‐1, Nrf2, and Bcl‐2, which had been reduced due to oxidative stress, inflammatory, and apoptotic pathways, while suppressing the elevated gene expression levels of NFκB, TNF‐α, Bax, and Cas‐3. Furthermore, SYA regulated the altered protein expression levels of Nrf2, Cas‐3, Bax, and Bcl‐2 induced by CYC. Microscopically, SYA also mitigated liver and kidney tissue damage caused by CYC. In conclusion, SYA significantly reduced CYC‐induced hepatonephrotoxicity by inhibiting inflammation, oxidative stress, and apoptosis by employing the Nrf2/NFκB/HO‐1 pathway. These findings indicate that SYA has the possibility as a treatment option agent in the case of prevention of liver and kidney damage.

ABSTRACTCisplatin (CIS) is a chemotherapeutic agent frequently used in cancer treatment. However, depending on the dosage and duration of use, CIS can lead to hepatotoxicity and nephrotoxicity. Iristectorin A (IRIS), a natural flavonoid, has been found to exhibit antioxidant and protective effects. In this paper, we scrutinized the effects and molecular mechanisms of the IRIS on CIS‐induced liver and kidney damage in mice. IRIS administration alleviated CIS‐induced elevations in AST, ALT, ALP, BUN, and creatinine levels by approximately 12%, 15%, 11%, 21%, and 15%, respectively. It also inhibited liver and kidney MDA levels by approximately 29% and 28%, while enhancing liver and kidney GSH, SOD, and CAT levels by 47%–60%, 85%–70%, and 90%–55%, respectively. IRIS enhanced liver and kidney mRNA expression levels of Nrf2 (by approximately 1.6‐ and 1.5‐fold, respectively), HO‐1 (by 1.5‐ and 1.5‐fold, respectively), and Bcl‐2 (by 1.5‐ and 1.4‐fold, respectively). In addition, IRIS suppressed the mRNA expression levels of NF‐κB (by 0.7‐ and 0.7‐fold), TNF‐α (by 0.7‐ and 0.7‐fold), Bax (by 0.8‐ and 0.7‐fold), and Cas‐3 (by 0.9‐ and 0.7‐fold). Protein expression analysis revealed that IRIS increased Nrf2 (by 1.5‐ to 1.2‐fold) and Bcl‐2 levels (by 1.3‐ to 1.7‐fold), and reduced Bax (by 0.7‐ to 0.8‐fold) and Cas‐3 (by 0.8‐ and 0.8‐fold) levels altered by CIS treatment. Moreover, IRIS administration prevented histopathological changes in the liver and kidney caused by CIS. Ultimately, IRIS was found to substantially mitigate CIS‐induced hepatorenal injury by targeting oxidative stress, inflammation, and apoptosis through regulation of the Nrf2/HO‐1 signaling pathway. Therefore, IRIS holds potential as a therapeutic adjuvant in the use of CIS.

Boron, found in nature in the form of compounds, has beneficial effects on the organism. However, information about the toxic effects of boron or its compounds is limited. This study aims to assess the effects of high dose boric acid on hormonal balance, oxidative stress, and DNA damage in female rats during the menstrual cycle. A total of 56 female Wistar albino rats were randomly allocated into two groups of equal size: a control group and a boric acid group (350 mg/kg, i.p.). These groups were subdivided into four subgroups based on the menstrual cycle phases (estrus, proestrus, diestrus, and metestrus), with seven rats in each subgroup. At the end of the 14-day experimental phase, biochemical, hormonal, and oxidative stress parameters and DNA damage on blood and tissue (liver, ovary, and kidney) samples were also studied. Additionally, histopathological examinations were performed on the liver, ovary, and kidney. High-dose boric acid did not affect biochemical parameters, including glucose, cholesterol, triglyceride, high-density lipoprotein, and low-density lipoprotein levels. However, it increased serum follicle-stimulating hormone levels, while luteinizing hormone, progesterone, and estrogen levels decreased. Furthermore, malondialdehyde levels were found to be elevated in blood, liver, and kidneys, whereas glutathione levels, as well as superoxide dismutase and catalase enzyme activities, were reduced. Although high-dose boric acid did not induce DNA damage, it caused mild tissue damage in the liver, ovary, and kidneys. These findings indicate that a high dose of boric acid induces oxidative stress and alters hormonal balance in female rats.

Pyraclostrobin, a strobilurin-derived fungicide, causes oxidative stress and DNA damage in the organism. Taurine plays an important role in metabolic processes such as osmoregulatory, cytoprotective, and antioxidant effects. The study aimed to investigate the protective effect of taurine in Sprague Dawley male rats exposed to pyraclostrobin. The rats were separated into 6 groups and were found 8 animals in each group. Rats were given 30 mg/kg pyraclostrobin and pyraclostrobin together with three different taurine concentrations (50, 100, and 200 mg/kg) via oral gavage for 28 days. While pyraclostrobin increased biochemical parameters, lipid peroxidation, and DNA damage, it decreased glutathione levels and enzyme activities of catalase and superoxide dismutase. Pyraclostrobin increased apoptotic, proinflammatory, and CYP2E1 mRNA expression levels, whereas antiapoptotic gene Bcl-2 mRNA expression levels decreased in liver tissue. Additionally, pyraclostrobin caused histopathological alterations in tissues. Taurine in a dose-dependent manner reversed the changes caused by pyraclostrobin. As a result, taurine exhibited a cytoprotective effect by showing antioxidant, anti-inflammatory, and antiapoptotic activities against oxidative damage caused by pyraclostrobin. Graphical Abstract

In the present study, we investigated the protective effect of magnolin (MAG) against oxidative stress induced by cyclophosphamide (CP) and its role in the Nrf2/HO-1 signaling pathway. Rats were administered MAG (1 mg/kg, i.p.) for 14 days and CP (75 mg/kg, i.p.) on the 14th day. CP administration increased tissue damage, as evidenced by elevated levels of transaminases (aspartate and alanine), alkaline phosphatase, and renal parameters (blood urea nitrogen and creatinine). Additionally, 8-hydroxy-2 '-deoxyguanosine and malondialdehyde levels were increased, whereas glutathione levels, along with catalase and superoxide dismutase activities, decreased in CP-treated rats. CP also down-regulated the expression of Bcl-2, HO-1, Nrf2, and NQO-1, while up-regulating Bax, Cas-3, TNF-alpha, Cox-2, iNOS, IL-6, IL-1 beta, and NF kappa B in liver and kidney tissues. In addition, CP treatment caused histopathological changes in heart, lung, liver, kidney, brain, and testis tissues. Treatment with MAG improved biochemical and oxidative stress parameters and prevented histopathological changes in CP-treated rats. Moreover, MAG suppressed the expression of inflammatory cytokines and apoptosis markers. In conclusion, MAG effectively prevented CP-induced toxicity by reducing oxidative stress, inflammation, and apoptosis, with its protective efficacy associated with the up-regulation of Nrf2/HO-1 signaling. Graphical Abstract

It is seen that cyclophosphamide, which is used in treating many diseases, especially cancer, causes toxicity in studies, and its metabolites induce oxidative stress. This study aimed to investigate the protective effects of resveratrol and Coenzyme Q10, known for their antioxidant properties, separately and together, against oxidative stress induced by cyclophosphamide. In this study, 35 Wistar albino male rats were divided into five groups. Groups; Control group, cyclophosphamide (CP) group (CP as 75 mg kg i.p. on day 14), coenzyme Q(10) (CoQ(10)) + CP group (20 mg/kg i.p. CoQ(10) + 75 mg kg i.p. CP), resveratrol (Res) + CP group (20 mg/kg i.p. Res + 75 mg/kg i.p. CP), CoQ(10) + Res + CP group (20 mg/kg i.p Res + 20 mg/kg i.p CoQ(10) and 75 mg/kg i.p.CP). At the end of the experiment, the cholesterol, creatinine and urea levels of the group given CP increased, while a decrease was observed in the groups given Res and CoQ10. Malondialdehyde level was high, glutathione level, superoxide dismutase and catalase activities were decreased in the blood and all tissues (liver, kidney, brain, heart and testis) of the CP given group. DNA damage and histopathological changes were also observed. In contrast, Res and CoQ(10), both separately and together, reversed the CP-induced altered level and enzyme activities and ameliorated DNA damage and histopathological changes. In this study, the effects of Res and CoQ(10) against CP toxicity were examined both separately and together. [GRAPHICS]

This study compares the physicochemical, photocatalytic, antimicrobial, toxicity and genotoxic properties of zinc oxide nanoparticles (ZnONPs) produced by hydrothermal and sol–gel methods as an alternative biomaterial. The comparative antibacterial activities, toxicity and DNA damage effects of ZnONPs on Drosophila melanogaster were determined using different doses. The study also investigates the effects of ZnONPs on malondialdehyde (MDA) and glutathione (GSH) levels, as well as superoxide dismutase (SOD) and catalase (CAT) activity. The structural, optical, and morphological properties of ZnONPs were investigated using X-ray diffractometer (XRD), UV–Visible spectrophotometry (UV–Vis), and field emission scanning electron microscopy (FESEM). The photocatalytic activity of ZnONPs in methylene blue solution was determined, and a high photocatalytic efficiency of 87 % was achieved in a short time. ZnONPs were found to have a significant antimicrobial effect on Streptococcus mutans ATCC 10449. Additionally, ZnONPs were non-toxic doses and did not cause DNA damage. In conclusion, ZnONPs synthesized can be safely used as filling material and bracket material especially in the field of dentistry since they are non-toxic, have a strong antimicrobial effect on S. mutans and do not cause DNA damage.

In this study, we investigated the occurrence of nitrofuran (NF) metabolites, namely 3-amino-2-oxazolidinone (AOZ), semicarbazide (SEM), 5-methylmorpholino-3-amino-2-oxazolidinone (AMOZ), and 1-aminohydantoin (AHD), in raw cow's milk and assessed the potential health risks to humans in the Ankara region, Turkey. The analytical methodology employed liquid chromatography coupled with tandem mass spectrometry (LC/MS/MS) to evaluate the milk samples. The results demonstrated that the methodological parameters, including linearity and recovery, along with other validation metrics, met the necessary criteria for the analysis. Raw milk samples collected from farms within Ankara province were subjected to LC-MS/MS analysis. Upon completion of the sample analyses, NF metabolites were not detected in any of the raw milk samples. Therefore, we conclude that the NF metabolites can be accurately quantified in milk using LC/MS/MS, and the milk available for consumption in this region does not present a health risk concerning NFs to consumers.