Sürdürülebilir Kalkınma Amaçları

• 3
• 1

• MakaleAçık Erişim2024Scopus SJRQ2/r/munzur/2006
  Effects of naringenin on oxidative damage and apoptosis in liver and kidney in rats subjected to chronic mercury chloride

  Kahramanoğullari, Merve; Erişir, Mine; Yaman, Mine; Parlak Ak, Tuba

  Mercury chloride is a type of heavy metal that causes the formation of free radicals, causing hepatotoxicity, nephrotoxicity and apoptosis. In this study, the effects of naringenin on oxidative stress and apoptosis in the liver and kidney of rats exposed to mercury chloride were investigated. In the study, 41 2-month-old male Wistar-Albino rats were divided into five groups. Accordingly, group 1 was set as control group, group 2 as naringenin-100, group 3 as mercury chloride, group 4 as mercury chloride + naringenin-50, and group 5 as mercury chloride + naringenin-100. For the interventions, 1 mL/kg saline was administered to the control, 0.4 mg/kg/day mercury (II) chloride to the mercury chloride groups by i.p., and 50 and 100 mg/kg/day naringenin prepared in corn oil to the naringenin groups by gavage. All the interventions lasted for 20 days. Mercury chloride administration was initiated 1 h following the administration of naringenin. When mercury chloride and the control group were compared, a significant increase in plasma urea, liver and kidney malondialdehyde (MDA) levels, in kidney superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) activities (p <.001), and a significant decrease in liver and kidney glutathione (GSH) levels (p <.001), in liver catalase (CAT) activity (p <.01) were observed. In addition, histopathological changes and a significant increase in caspase-3 levels were detected (p <.05). When mercury chloride and treatment groups were compared, the administration of naringenin caused a decrease aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH) (p <.01), urea, creatinine levels (p <.001) in plasma, MDA levels in liver and kidney, SOD, GSH-Px, GST activities in kidney (p <.001), and increased GSH levels in liver and kidney. The addition of naringenin-100 increased GSH levels above the control (p <.001). The administration of naringenin was also decreased histopathological changes and caspase-3 levels (p <.05). Accordingly, it was determined that naringenin is protective and therapeutic against mercury chloride-induced oxidative damage and apoptosis in the liver and kidney, and 100 mg/kg naringenin is more effective in preventing histopathological changes and apoptosis.

  • 
  AtıfScopus13·WoS14·OpenAlex14

  İncele
• MakaleYalnız künye2020Scopus SJRQ2/r/munzur/3674
  Assessment of impact of α-Fe2O3 and γ-Fe2O3 nanoparticles on phytoplankton species Selenastrum capricornutum and Nannochloropsis oculata

  Ates, Mehmet; Cimen, Isil C. C.; Unal, Ilkay; Kutlu, Banu; Ertit Tastan, Burcu; Danabas, Durali; Aksu, Onder; Arslan, Zikri

  In this study, the impact of alpha-iron oxide (α-Fe2O3, 20-40 nm) and gamma iron oxide (γ-Fe2O3, 20-40 nm) nanoparticles (NPs) on phytoplankton species Selenastrum capricornutum and Nannochloropsis oculata was investigated Characterizations of the NPs were systematically carried out by TEM, dynamic light scattering, zeta potential, X-ray diffraction, SEM, and Fourier transformation infrared spectroscopy. Acute toxicity was tested between 0.2 and 50 mg/L for each NP for a period of 72 hours exposure. γ-Fe2O3 NP inhibited development of N oculata at the rate of 54% in 0.2 mg/L group with a high mortality rate of up to 82%. α-Fe2O3 NPs were less toxic that induced 97% mortality on N oculata at 10 mg/L suspensions. In contrast, α-Fe2O3 NP inhibited growth of S capricornutum strongly (73%) in 0.2 mg/L group. γ-Fe2O3 NPs showed similar growth inhibition (72%) on S capricornutum in 10 mg/L suspensions. Despite the differential effects, the results indicated acute toxicity of α-Fe2O3 and γ-Fe2O3 NPs on N oculata and S capricornutum.

  AtıfScopus27·WoS20·OpenAlex25

  İncele
• MakaleAçık Erişim2017Scopus SJRQ2/r/munzur/4267
  Effects of subchronic exposure to zinc nanoparticles on tissue accumulation, serum biochemistry, and histopathological changes in tilapia (Oreochromis niloticus)

  Kaya, Hasan; Duysak, Muge; Akbulut, Mehmet; Yilmaz, Sevdan; Guerkan, Mert; Arslan, Zikri; Demir, Veysel; Ates, Mehmet

  Zinc nanoparticles (ZnNPs) are among the least investigated NPs and thus their toxicological effects are not known. In this study, tilapia (Oreochromis niloticus) were exposed to 1 and 10 mg/L suspensions of small size (SS, 40-60 nm) and large size (LS, 80-100 nm) ZnNPs for 14 days under semi-static conditions. Total Zn levels in the intestine, liver, kidney, gill, muscle tissue, and brain were measured. Blood serum glucose (GLU), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and lactate dehydrogenase (LDH) were examined to elucidate the physiological disturbances induced by ZnNPs. Organ pathologies were examined for the gills, liver, and kidney to identify injuries associated with exposure. Significant accumulation was observed in the order of intestine, liver, kidney, and gills. Zn levels exhibited time- and concentration-dependent increase in the organs. Accumulation in kidney was also dependent on particle size; NPs SS-ZnNPs were trapped more effectively than LS-ZnNPs. No significant accumulation occurred in the brain (p>0.05) while Zn levels in muscle tissue increased only marginally (p0.05). Significant disturbances were noted in serum GOT and LDH (p<0.05). The GPT levels fluctuated and were not statistically different from those of controls (p>0.05). Histopathological tubular deformations and mononuclear cell infiltrations were observed in kidney sections. In addition, an increase in melano-macrophage aggregation intensity was identified on the 7th day in treatments exposed to LS-ZnNPs. Mononuclear cell infiltrations were identified in liver sections for all treatments. Both ZnNPs caused basal hyperplasia in gill sections. Fusions appeared in the gills after the 7th day in fish treated with 10 mg/L suspensions of SS-ZnNPs. In addition, separations in the secondary lamella epithelia were observed. The results indicated that exposure to ZnNPs could lead to disturbances in blood biochemistry and cause histopathological injuries in the tissues of O. niloticus. (c) 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1213-1225, 2017.

  • 
  AtıfWoS22·OpenAlex28

  İncele
• MakaleAçık Erişim2015Scopus SJRQ2/r/munzur/4103
  Accumulation and Toxicity of CuO and ZnO Nanoparticles Through Waterborne and Dietary Exposure of Goldfish (Carassius auratus)

  Ates, Mehmet; Arslan, Zikri; Demir, Veysel; Daniels, James; Farah, Ibrahim O.

  Dietary and waterborne exposure to copper oxide (CuO) and zinc oxide (ZnO) nanoparticles (NPs) was conducted using a simplified model of an aquatic food chain consisting of zooplankton (Artemia salina) and goldfish (Carassius auratus) to determine bioaccumulation, toxic effects, and particle transport through trophic levels. Artemia contaminated with NPs were used as food in dietary exposure. Fish were exposed to suspensions of the NPs in waterborne exposure. ICP-MS analysis showed that accumulation primarily occurred in the intestine, followed by the gills and liver. Dietary uptake was lower, but was found to be a potential pathway for transport of NPs to higher organisms. Waterborne exposure resulted in about a 10-fold higher accumulation in the intestine. The heart, brain, and muscle tissue had no significant Cu or Zn. However, concentrations in muscle increased with NP concentration, which was ascribed to bioaccumulation of Cu and Zn released from NPs. Free Cu concentration in the medium was always higher than that of Zn, indicating CuO NPs dissolved more readily. ZnO NPs were relatively benign, even in waterborne exposure (p0.05). In contrast, CuO NPs were toxic. Malondialdehyde levels in the liver and gills increased substantially (p<0.05). Despite lower Cu accumulation, the liver exhibited significant oxidative stress, which could be from chronic exposure to Cu ions. (c) 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 119-128, 2015.

  • 
  • 
  AtıfWoS92·OpenAlex99

  İncele
• MakaleÖn baskısı açık2015Scopus SJRQ2/r/munzur/4100
  Evaluation of Alpha and Gamma Aluminum Oxide Nanoparticle Accumulation, Toxicity, and Depuration in Artemia salina Larvae

  Ates, Mehmet; Demir, Veysel; Arslan, Zikri; Daniels, James; Farah, Ibrahim O.; Bogatu, Corneliu

  In this study, Artemia salina (crustacean filter feeders) larvae were used as a test model to investigate the toxicity of aluminum oxide nanoparticles (Al2O3 NPs) on marine microorganisms. The uptake, toxicity, and elimination of -Al2O3 (50 nm and 3.5 m) and -Al2O3 (5 nm and 0.4 m) NPs were studied. Twenty-four and ninety-six hour exposures of different concentrations of Al2O3 NPs to Artemia larvae were conducted in a seawater medium. When suspended in water, Al2O3 NPs aggregated substantially with the sizes ranging from 6.3 nm to >0.3 mu m for spherical NPs and from 250 to 756 nm for rod-shaped NPs. The phase contrast microscope images showed that NPs deposited inside the guts as aggregates. Inductively coupled plasma mass spectrometry analysis showed that large particles (3.5 m -Al2O3) were not taken up by Artemia, whereas fine NPs (0.4 m -Al2O3) and ultra-fine NPs (5 nm -Al2O3 and 50 nm -Al2O3) accumulated substantially. Differences in toxicity were detected as changing with NP size and morphology. The malondialdehyde levels indicated that smaller -Al2O3 (5 nm) NPs were more toxic than larger -Al2O3 (0.4 mu m) particulates in 96 h. The highest mortality was measured as 34% in 96 h for -Al2O3 NPs (5 nm) at 100 mg/L (LC50 > 100 mg/L). -Al2O3 NPs were more toxic than -Al2O3 NPs at all conditions. (c) 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 109-118, 2015.

  AtıfWoS65·OpenAlex84

  İncele