Browsing by Author "Tüfekci, K.K."

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An investigation of the distributions of ferroptosis and necroptosis mediators in the maternal–fetal interface at different days of rat pregnancy
(John Wiley and Sons Inc, 2024) Tatar, M.; Tüfekci, K.K.
Ferroptosis and necroptosis are recognized as playing major roles in the regulation of various physiological processes. However, the physiological role of the cell death mediated by these two pathways in the developmental process has not yet been clearly established. This study investigated ferroptosis and necroptosis signalling pathways in maternal–fetal tissue in the different gestational days (GD) of rat pregnancy using immunohistochemical and western blot methods in order to fill this gap. Twenty-four female Wistar albino rats were mated and divided into three groups. Maternal–fetal tissue samples were collected on GD 5, 12 and 19 of pregnancy. Expression and total protein levels of the markers glutathione peroxidase-4, soluble transporter family 7 member 11, transferrin receptor, receptor-interacting serine/threonine-protein kinase 1, receptor-interacting serine/threonine-protein kinase 3 and mixed lineage kinase domain-like protein were investigated on both the maternal and fetal surfaces of the placenta using immunohistochemical and western blot methods. The results showed varying levels of protein expression of both ferroptosis and necroptosis mediators in the GD 5, 12 and 19 of pregnancy. Immunohistochemical analyses revealed that these mediators were located on both the maternal (decidua and metrial gland) and fetal surfaces (labyrinth zone, yolk sac and basal zone) and that their expression levels changed in the different GD. The findings revealed the existence of important ferroptosis and necroptosis pathway mediators in rat maternal–fetal tissue. These results may provide a molecular framework for a better understanding of the communication between the placenta, decidua and fetus during the developmental process.
An investigation of the distributions of ferroptosis and necroptosis mediators in the maternal-fetal interface at different days of rat pregnancy
(2023.01.01) Tatar, M.; Tüfekci, K.K.
Ferroptosis and necroptosis are recognized as playing major roles in the regulation of various physiological processes. However, the physiological role of the cell death mediated by these two pathways in the developmental process has not yet been clearly established. This study investigated ferroptosis and necroptosis signalling pathways in maternal-fetal tissue in the different gestational days (GD) of rat pregnancy using immunohistochemical and western blot methods in order to fill this gap. Twenty-four female Wistar albino rats were mated and divided into three groups. Maternal-fetal tissue samples were collected on GD 5, 12 and 19 of pregnancy. Expression and total protein levels of the markers glutathione peroxidase-4, soluble transporter family 7 member 11, transferrin receptor, receptor-interacting serine/threonine-protein kinase 1, receptor-interacting serine/threonine-protein kinase 3 and mixed lineage kinase domain-like protein were investigated on both the maternal and fetal surfaces of the placenta using immunohistochemical and western blot methods. The results showed varying levels of protein expression of both ferroptosis and necroptosis mediators in the GD 5, 12 and 19 of pregnancy. Immunohistochemical analyses revealed that these mediators were located on both the maternal (decidua and metrial gland) and fetal surfaces (labyrinth zone, yolk sac and basal zone) and that their expression levels changed in the different GD. The findings revealed the existence of important ferroptosis and necroptosis pathway mediators in rat maternal-fetal tissue. These results may provide a molecular framework for a better understanding of the communication between the placenta, decidua and fetus during the developmental process.
An investigation of the endoplasmic reticulum stress in obesity exposure in the prenatal period
(2023.01.01) Tüfekci, K.K.; Tatar, M.; Terzi, F.; Bakirhan, E.G.
Objectives: Exposure to maternal obesity has been shown to make offspring more prone to cognitive and metabolic disorders later in life. Although the underlying mechanisms are unclear, the role of endoplasmic reticulum (ER) stress in the fetal programming process is remarkable. ER stress can be activated by many chronic diseases, including obesity and diabetes. Therefore, our study aimed to investigate the role of ER stress caused by maternal diet-induced obesity in the offspring hippocampus. We also evaluated the protective effect of N-acetylcysteine (NAC) against ER stress.Methods: A rat obesity model was created by providing a high-fat (60 % kcal) diet. N-acetylcysteine (NAC) was administered at a dosage of 150 mg/kg via the intragastric route. The animals were mated at the age of 12 weeks. The same diet was maintained during pregnancy and lactation. The experiment was terminated on the postnatal 28th day, and the offspring's brain tissues were examined. Immunohistochemical staining for ER stress markers was performed on sections taken from tissues after routine histological procedures.Results: The results revealed increased GRP78, PERK, and eIF2 alpha immunoreactivities in the hippocampal dentate gyrus (DG) and cornu ammonis 1 (CA1) regions in the obese group offspring, while the expression of those markers in those regions normalized with NAC supplementation (p < 0.01). Statistical analysis of XBP1 immunoreactivity H-scores revealed no difference between the study groups (p > 0.05).Discussion: These results suggest that exposure to obesity during the prenatal period may cause increased ER stress in hippocampal neurons, which have an important role in the regulation of learning, memory and behavior, and this may contribute to decreased cognitive performance. On the other hand, NAC stands out as an effective agent that can counteract hippocampal ER stress.
An investigation of the endoplasmic reticulum stress in obesity exposure in the prenatal period
(Elsevier, 2023) Tüfekci, K.K.; Tatar, M.; Terzi, F.; Bakirhan, E. G.
Objectives: Exposure to maternal obesity has been shown to make offspring more prone to cognitive and metabolic disorders later in life. Although the underlying mechanisms are unclear, the role of endoplasmic reticulum (ER) stress in the fetal programming process is remarkable. ER stress can be activated by many chronic diseases, including obesity and diabetes. Therefore, our study aimed to investigate the role of ER stress caused by maternal diet-induced obesity in the offspring hippocampus. We also evaluated the protective effect of N-acetylcysteine (NAC) against ER stress. Methods: A rat obesity model was created by providing a high-fat (60% kcal) diet. Nacetylcysteine (NAC) was administered at a dosage of 150 mg/kg via the intragastric route. The animals were mated at the age of 12 weeks. The same diet was maintained during pregnancy and lactation. The experiment was terminated on the postnatal 28th day, and the offspring's brain tissues were examined. Immunohistochemical staining for ER stress markers was performed on sections taken from tissues after routine histological procedures. Results: The results revealed increased GRP78, PERK, and eIF2α immunoreactivities in the hippocampal dentate gyrus (DG) and cornu ammonis 1 (CA1) regions in the obese group offspring, while the expression of those markers in those regions normalized with NAC supplementation (p<0.01). Statistical analysis of XBP1 immunoreactivity H-scores revealed no difference between the study groups (p>0.05). Discussion: These results suggest that exposure to obesity during the prenatal period may cause increased ER stress in hippocampal neurons, which have an important role in the regulation of learning, memory and behavior, and this may contribute to decreased cognitive performance. On the other hand, NAC stands out as an effective agent that can counteract hippocampal ER stress.
Oleuropein Mitigates Acrylamide-Induced Nephrotoxicity by Affecting Placental Growth Factor Immunoactivity in the Rat Kidney
(2023-10) Tüfekci, K.K.; Tatar, M.
The liver is susceptible to toxic effects, as it is the main site of acrylamide biotransformation and detoxification. Researchers have claimed that placental growth factor (PlGF) and its pathway are potentially involved in numerous diseases, including liver fibrosis and angiogenesis. Oleuropein is a natural phenolic compound with potent antioxidant effects. The purpose of this study was to examine the role of PlGF and the potential protection provided by oleuropein in acrylamide hepatotoxicity. Wistar albino rats were assigned into control, acrylamide (ACR) (5 mg/kg), oleuropein (OLE) (4.2 mg/kg), and ACR+OLE groups. Acrylamide and oleuropein were administered for 21 days. The control group received only physiological saline. Liver tissues were evaluated histologically and immunohistochemically. Histological examinations revealed significant enlargement of the sinusoidal vessels and abundant hepatocytes with pyknotic nuclei in the ACR group. Acrylamide toxicity resulted in elevated PlGF, accumulation of 8-hydroxydeoxyguanosine (8-OHdG), and increased Caspase-3 immunoreactivity in the liver. Oleuropein treatment reduced the increased expression of PlGF, 8-OHdG, and Caspase-3 against these deleterious effects observed in the ACR group. A positive correlation was observed between PlGF levels as well as oxidative stress and apoptosis markers in acrylamide toxicity. Oleuropein probably counteracted this mechanism by exhibiting antioxidant activity.
Oleuropein Mitigates Acrylamide-Induced Nephrotoxicity by Affecting Placental Growth Factor Immunoactivity in the Rat Kidney
(2023.01.01) Tüfekci, K.K.; Tatar, M.
Objective: Oleuropein is one of the main components of the antioxidant properties of olive leaves. Placental growth factor is an important regulator in angiogenesis and inflammation, its levels being variable in pathological conditions. In this study, we aimed to examine changes in placental growth factor expression and the effect of oleuropein, found in olive leaves, in rats exposed to acrylamide nephrotoxicity. Material and Methods: Twenty-four male Wistar albino rats were allocated into 4 groups. The control group received saline solution only. The oleuropein group received oleuropein (4.2 mg/kg), the acrylamide group received acrylamide (5 mg/kg), and the acrylamide and oleuropein group received acrylamide (5 mg/kg) and oleuropein (4.2 mg/kg). All substances were administered via gastric gavage for 21 days. Kidney tissues were removed at the end of the study and subjected to histopathological, stereological, and immunohistochemical procedures. Results: Histopathological examination revealed dilatation, vacuolization, and degeneration in the proximal and distal tubules and increased placental growth factor immunoreactivity in the acrylamide group. Cavalieri volume analysis revealed increased cortex, distal, and proximal tubule volumes (P < .01). Conclusion: Oleuropein significantly attenuated acrylamide-induced kidney injury by altering placental growth factor immunoreactivity. Placental growth factor immunoreactivity can be used as a marker of acryl-amide nephrotoxicity, and oleuropein may counteract acrylamide-induced kidney injury.
Preliminary study on the impact of 900 MHz radiation on human sperm: An in vitro molecular approach
(Elsevier Inc., 2024) Keskin, I.; Karabulut, S.; Kaplan, A.A.; Alagöz, M.; Akdeniz, M.; Tüfekci, K.K.; Davis, D.L.; Kaplan, S.
The use of technologies that produce and emit electromagnetic fields (EMF) is growing exponentially worldwide. The biological effects of EMF-emitting equipment, such as mobile phones and other wireless devices, have been studied in the last decade using in vitro and in vivo methods. Infertility is a growing health problem, and nearly half of cases are because of male-factor. This study investigated the direct in vitro effects of 900 MHz radiation exposure on sperm parameters, genetic status, apoptotic markers, and the PI3K/AKT signaling pathway in healthy normozoospermic men. Semen samples were divided into four groups, two control (30 min and 1 h) and two EMF exposure (30 min and 1 h). Sperm parameters (motility, progressive motility, acrosomal index, morphology), genetic status (DNA fragmentation and chromatin integrity), apoptotic markers (cytokine-c and caspase-3 expression) and the PI3K/AKT signaling pathway (phosphoinoitide 3-kinase-PI3K- and phosphorylated AKT- p-AKT-) were analysed. Sperm motility were significantly reduced in 30 min EMF exposure while a significant increase in the expression of p-AKT were observed in 1 h EMF exposure group. An increased vacuolisation, acrosomal defect, extension of subacrosomal space, uncondensed chromatin structure, apoptotic signs and disrupted axoneme were observed in both EMF groups which were not observed in the control group. Other sperm parameters (morphology and acrosomal index), genetic status, apoptotic markers and the PI3K expression rates had no significant change.
Preliminary study on the impact of 900 MHz radiation on human sperm: An in vitro molecular approach
(2024.01.01) Keskin, I.; Karabulut, S.; Kaplan, A.A.; Alagöz, M.; Akdeniz, M.; Tüfekci, K.K.; Davis, D.L.; Kaplan, S.
The use of technologies that produce and emit electromagnetic fields (EMF) is growing exponentially worldwide. The biological effects of EMF-emitting equipment, such as mobile phones and other wireless devices, have been studied in the last decade using in vitro and in vivo methods. Infertility is a growing health problem, and nearly half of cases are because of male-factor. This study investigated the direct in vitro effects of 900 MHz radiation exposure on sperm parameters, genetic status, apoptotic markers, and the PI3K/AKT signaling pathway in healthy normozoospermic men. Semen samples were divided into four groups, two control (30 min and 1 h) and two EMF exposure (30 min and 1 h). Sperm parameters (motility, progressive motility, acrosomal index, morphology), genetic status (DNA fragmentation and chromatin integrity), apoptotic markers (cytokine-c and caspase-3 expression) and the PI3K/AKT signaling pathway (phosphoinoitide 3-kinase-PI3K- and phosphorylated AKT- p-AKT-) were analysed. Sperm motility were significantly reduced in 30 min EMF exposure while a significant increase in the expression of p-AKT were observed in 1 h EMF exposure group. An increased vacuolisation, acrosomal defect, extension of subacrosomal space, uncondensed chromatin structure, apoptotic signs and disrupted axoneme were observed in both EMF groups which were not observed in the control group. Other sperm parameters (morphology and acrosomal index), genetic status, apoptotic markers and the PI3K expression rates had no significant change.
Preliminary Study on the Impact of 900MHz Radiation on Human Sperm: An In Vitro Molecular Approach
(2024) Keskin, I.; Karabulut, S.; Kaplan, A.A.; Alagöz, M.; Akdeniz, M.; Tüfekci, K.K.; Davis, D.L.; Kaplan, S.
The use of technologies that produce and emit electromagnetic fields (EMF) is growing exponentially worldwide. The biological effects of EMF-emitting equipment, such as mobile phones and other wireless devices, have been studied in the last decade using in vitro and in vivo methods. Infertility is a growing health problem, and nearly half of cases are because of male-factor. This study investigated the direct in vitro effects of 900MHz radiation exposure on sperm parameters, genetic status, apoptotic markers, and the PI3K/AKT signaling pathway in healthy normozoospermic men. Semen samples were divided into four groups, two control (30min and 1h) and two EMF exposure (30min and 1h). Sperm parameters (motility, progressive motility, acrosomal index, morphology), genetic status (DNA fragmentation and chromatin integrity), apoptotic markers (cytokine-c and caspase-3 expression) and the PI3K/AKT signaling pathway (phosphoinoitide 3-kinase-PI3K- and phosphorylated AKT- p-AKT-) were analysed. Sperm motility were significantly reduced in 30min EMF exposure while a significant increase in the expression of p-AKT were observed in 1h EMF exposure group. An increased vacuolisation, acrosomal defect, extension of subacrosomal space, uncondensed chromatin structure, apoptotic signs and disrupted axoneme were observed in both EMF groups which were not observed in the control group. Other sperm parameters (morphology and acrosomal index), genetic status, apoptotic markers and the PI3K expression rates had no significant change.