High Carbohydrate, Fat, and Protein Diets Have a Critical Role in Folliculogenesis and Oocyte Development in Rats.

To date, there is no comparative data on the effects of carbohydrates, fat, and proteins, which are macronutrients, on female reproductive functions. Therefore, in this study, we investigated the effects of diets enriched with carbohydrates, fats, and proteins on folliculogenesis and oocyte development in female rats. 21-day-old rats that were just weaned were divided into 4 groups: control, carbohydrate, fat, and protein. The control group was fed with standard chow and the carbohydrate, fat, and protein groups were fed diets enriched with 75% carbohydrate, 60% fat, and 50% protein for 11 weeks, respectively. It was found that high-fat and high-protein diets caused an increase in the estrous cycle length compared to carbohydrate group (p < 0.05). Graafian follicle number decreased in the protein group compared to the control (p < 0.05). However, the atretic follicle number was higher in the fat group compared to the control group (p < 0.05). In the carbohydrate group, Zp1 was found to be lower than the control and protein groups, Zp2 was found to be lower than the control, and Zp3 was found to be lower than the fat group (p < 0.05). While BMP15 was similar between groups (p > 0.05), GDF9 was lower in all diet groups compared to the control (p < 0.05). Foxo3a was lower in the protein group compared to carbohydrate and control (p < 0.05). GAS2 was found to be higher in the control group than the fat group, and higher in the carbohydrate group than the fat and protein groups (p < 0.05). FSH, LH, Progesterone, and E2 levels were higher in all three diet groups than in the control (p < 0.05). Also, significant differences were observed between the groups regarding adiponectin, resistin, and leptin levels. Taken together, high carbohydrate, fat, and protein intake are associated with impairment of the menstrual cycle, depletion of the developing follicle types, and altered expression of folliculogenesis-specific genes and hormones. Therefore, long-term macronutrient diets may result in shortened reproductive periods and reduced fertilization potential in females in the long run.

Phoenixin-14 may ameliorate testicular damage caused by torsion-detorsion by reducing oxidative stress and inflammation in prepubertal rats.

The present study aimed to investigate the effects of Phoenixin-14 (PNX-14) on oxidative damage, inflammatory response, histopathological variations, and serum testosterone levels in testicular tissues. Forty-eight Wistar albino prepubertal male rats were divided into 4 groups (Sham, TTD, TT+PNX+TD, TTD+PNX) (n=12). The torsion period was 2 hours and the detorsion period was 24 hours in the testicular torsion/detorsion (TD) groups. A single PNX-14 (50 µg/kg) dose was injected into the rats in the TT+PNX TD group on the 90th minute of torsion, and it was injected into the rats in the TTD+PNX group at the beginning of detorsion. Oxidative damage in testicular tissues was determined based on superoxide dismutase (SOD), malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS), and inflammatory damage was determined based on TNF-α and IL-6 levels. Histopathological variations were investigated with the Periodic Acid Schiff (PAS) staining method in testicular tissues and analyzed based on Johnsen scores. Spermatogonia cells were examined immunohistochemically. Serum testosterone levels were determined with the enzyme-linked immunosorbent assay (ELISA). A significant increase in oxidative stress and inflammation parameters was determined in the TTD group when compared to the other groups (p<0.05). PNX-14 treatment led to a statistically significant decrease in these parameters and significantly repaired the TD damage in testicular tissue (p<0.05). Johnsen scoring revealed significant improvement in PNX-14 groups and an increase in spermatogonia count, supporting the biochemical findings (p<0.05). PNX-14 could be a potential therapeutic agent in testicular TD damage and further studies should be conducted to elucidate the present study findings.

Intracerebroventricular BDNF infusion may reduce cerebral ischemia/reperfusion injury by promoting autophagy and suppressing apoptosis.

Here, it was aimed to investigate the effects of intracerebroventricular (ICV) Brain Derived Neurotrophic Factor (BDNF) infusion for 7 days following cerebral ischemia (CI) on autophagy in neurons in the penumbra. Focal CI was created by the occlusion of the right middle cerebral artery. A total of 60 rats were used and divided into 4 groups as Control, Sham CI, CI and CI + BDNF. During the 7-day reperfusion period, aCSF (vehicle) was infused to Sham CI and CI groups, and BDNF infusion was administered to the CI + BDNF group via an osmotic minipump. By the end of the 7th day of reperfusion, Beclin-1, LC3, p62 and cleaved caspase-3 protein levels in the penumbra area were evaluated using Western blot and immunofluorescence. BDNF treatment for 7 days reduced the infarct area after CI, induced the autophagic proteins Beclin-1, LC3 and p62 and suppressed the apoptotic protein cleaved caspase-3. Furthermore, rotarod and adhesive removal test times of BDNF treatment started to improve from the 4th day, and the neurological deficit score from the 5th day. ICV BDNF treatment following CI reduced the infarct area by inducing autophagic proteins Beclin-1, LC3 and p62 and inhibiting the apoptotic caspase-3 protein while its beneficial effects were apparent in neurological tests from the 4th day.

Acrylamide, Applied During Pregnancy and Postpartum Period in Offspring Rats, Significantly Disrupted Myelination by Decreasing the Levels of Myelin-Related Proteins: MBP, MAG, and MOG.

Acrylamide (ACR) is a colorless, odorless, and water-soluble solid molecule. In addition to being an important industrial material, ACR is found in fried and baked carbohydrate-rich foods. ACR is regarded as a typical axonal neurotoxin that induces neuropathy. The brain is protected from oxidative damage by vitamin E, which is regarded as the most powerful fat-soluble antioxidant vitamin. This study aimed to reveal the toxic effect of ACR on the development of myelin in the brain at the molecular level and to examine whether Vitamin E has a neuroprotective effect on the harmful effect of ACR. The study was started by dividing 40 pregnant rats into 4 groups and after lactation, the study was continued with offspring rats (females and males offspring rats) from each group. Offspring rats were equally divided into Control, Vitamin E, ACR, ACR + Vitamin E groups. Following the ACR administration, the Water Maze test was applied to evaluate cognitive function. To evaluate the level of demyelination and remyelination, MBP, MAG, and MOG proteins and mRNA levels were performed. In addition, the degeneration of myelin and glial cells was examined by immunohistochemistry and electron microscopic analysis. Analysis results showed that ACR administration decreased gene and protein levels of myelin-related proteins MBP, MAG, and MOG. The findings were confirmed by histopathological, immunohistochemical, and microscopic examinations. The application of vitamin E improved this negative effect of ACR. It has been observed that ACR may play a role in the pathogenesis of myelin-related neurodegenerative diseases by causing demyelination during gestation, lactation, and post-lactation. In addition, it has been understood that vitamin E supports myelination as a strong neuroprotective vitamin against the toxicity caused by ACR. Our research results suggest that acrylamide may play a role in the etiopathogenesis of demyelinating diseases such as multiple sclerosis in humans since fast-food-type nutrition is very common today and people are chronically exposed to acrylamide.

96th-hour impact of scalding burns on end organ damage, systemic oxidative stress, and wound healing in rats treated with three different types of dressings.

In this study, we investigated the effects of three different burn dressing treatments, including experimental, silver, and modern dressing materials, on systemic oxidative stress in rats with severe scald burns within the first 96 h. The rats were divided into five groups: a burn group (n = 10), a polylactic membrane (PLM) group (n = 10), a silver sulfadiazine (SSD) group (n = 10), a curcumin group (n = 10), and a control group (n = 10), consisting of equal numbers of female and male rats. In the first four groups, 30% of the rats' total body surface area was scalded at 95°C. The burn group was not treated. Each group was treated with group-name dressing material. The control group was neither treated nor burned. The rats were sacrificed, and blood and tissue samples were obtained at the 96th hour when severe effects of oxidative stress developed postburns. Systemic inflammatory biomarkers and oxidative stress parameters were examined. In addition, apoptosis and organ damage in liver, kidney, lung, and skin tissues were evaluated biochemically and histopathologically. When the parameters were statistically analyzed, we found that systemic levels of oxidative stress and inflammatory damage to liver, kidney, and lung tissues were lower in the three treated groups than in the burn group. We believe that the dressing material's efficacy in the treatment of severe burns may be dependent on its ability to combat oxidative stress and inflammation.

Melatonin Attenuates Cerebral Ischemia/Reperfusion Injury through Inducing Autophagy.

INTRODUCTION: The aim of this study was to investigate how melatonin administration for 3 days or 7 days following cerebral ischemia (CI) injury would affect autophagy and, therefore, survival in neurons of the penumbra region. Moreover, it was also aimed at determining how this melatonin treatment would affect the neurological deficit score and rotarod and adhesive removal test durations. METHODS: Focal CI (90 min) was achieved in a total of 105 rats utilizing a middle cerebral artery occlusion model. After the start of reperfusion, the groups were treated with melatonin (10 mg/kg/day) for 3 days or 7 days. In all groups, neurological deficit scoring, rotarod, and adhesive removal tests were executed during reperfusion. Infarct areas were determined by TTC (2,3,5-triphenyltetrazolium chloride) staining at the end of the 3rd and 7th days of reperfusion. Beclin-1, LC3, p62, and caspase-3 protein levels were assessed using Western blot and immunofluorescence methods in the brain tissues. Moreover, penumbra areas were evaluated by transmission electron microscopy (TEM). RESULTS: Following CI, it was observed that melatonin treatment improved the rotarod and adhesive removal test durations from day 5 and reduced the infarct area after CI. It also induced autophagic proteins Beclin-1, LC3, and p62 and suppressed the apoptotic protein cleaved caspase-3. According to TEM findings, melatonin treatment partially reduced the damage in neurons after CI. CONCLUSION: Melatonin treatment following CI reduced the infarct area and induced the autophagic proteins Beclin-1, LC3, and p62 by inhibiting the apoptotic caspase-3 protein. The functional reflection of melatonin treatment on neurological test scores was became significant from the 5th day onward.

Histopathological and ultra-structural investigation of the damaging effects of hypoinsulinemia, hyper glycaemia and oxidative stress caused by parenteral nutrition combined with fasting on the small intestine of rabbits.

BACKGROUND AND STUDY AIMS: Parenteral nutrition (PN) is a life-saving practice when the use of the gastrointestinal tract is not appropriate. Despite its great benefits, however, PN may cause several complications. In this study, we conducted histopathological and ultra-structural examinations of the effect of PN combined with starvation on the small intestines of rabbits. MATERIALS AND METHODS: Rabbits were divided into four groups. A fasting + PN group was left completely unfed and received all its daily required energy by PN through an intravenous central catheter. An oral feeding + PN group received half the necessary daily calories by oral feeding and the other half through PN. A semi-starvation group received only half the necessary daily calories by oral feeding and no PN. The fourth group, serving as a control, was supplied with its entire daily energy requirements through oral feeding. After 10 days, the rabbits were euthanized. Blood and small intestine tissue samples were collected from all groups. Blood samples were biochemically analysed, and tissue samples were examined by light and transmission electron microscopy. RESULTS: The fasting + PN group exhibited lower insulin levels, higher glucose levels, and increased systemic oxidative stress than the other groups. Ultra-structural and histopathological examinations revealed a significant increase in apoptotic activity in this group's small intestines and a significant decrease in villus length and crypt depth. Severe damage to the intracellular organelles and nuclei of enterocytes was also observed. CONCLUSION: PN combined with starvation appears to cause apoptosis in the small intestine due to oxidative stress and hyperglycaemia with hypoinsulinemia, with destructive effects on small intestine tissue. Adding enteral nutrition to PN may reduce these destructive effects.

Biochemical and histopathological investigation of the protective effects of melatonin and vitamin E against the damage caused by acetamiprid in Balb-c mouse testicles at light and electron microscopic level.

The protective effects of melatonin (Mel) and vitamin E (Vit E) against the negative effects of acetamiprid (Acmp) on testicles, reproductive hormones, and oxidative stress parameters were investigated in the present study. A total of 50 Balb-c male mice were used in 7 groups; 6 mice in the control groups (distilled water, corn oil, ethanol), and 8 in other groups (Acmp, Acmp + Mel, Acmp + Vit E, Acmp + Vit E + Mel). After the experiment, which lasted 21 days, hematoxylin eosin (H&E), periodic acid Schiff (PAS), and caspase-3 immunohistochemical (IHC) staining was performed on the testicular tissues. Also, the tissues were examined ultrastructurally with the transmission electron microscopy (TEM). In the Acmp group, there were decreased seminiferous tubule diameter and epithelial thickness, epithelial degeneration, decreased spermatozoa in the lumen, decreased PAS-positive staining in the seminiferous epithelial basement membrane, edema in the interstitial area, and hydropic degeneration in Leydig cells. Caspase-3 immunoreactivity was higher than in the other groups. TEM examination showed degeneration in tubule cells, lysosomal accumulation in cells of the spermatogenic line, vacuolizations with myelin figures, and necrosis. Hydropic degeneration, electron-dense lipid vacuoles, and chromatolysis were evident in the Leydig cell cytoplasm. In Sertoli cells, electron-dense lysosomal deposits were noted. In biochemical terms, there were decreased tissue glutathione (GSH) and total antioxidant status (TAS), and increased malondialdehyde (MDA) and total oxidant status (TOS). Plasma luteinizing hormone (LH), follicular stimulating hormone (FSH), and testosterone levels were decreased. In the groups with melatonin, vitamin E, and both were applied together, tissue damage, and apoptotic cell death were reduced at both light microscopic and ultrastructural levels. In biochemical terms, there were decreased oxidative parameters and increased hormonal parameters. It was found that vitamin E was more effective in decreasing oxidative parameters and increasing antioxidative parameters when compared to melatonin, and hormonal parameters increased at a higher level in the Acmp + Vit E group than in all groups. As a result, it was found that exposure to Acmp caused damage to testicular tissue, induced oxidative stress in testicles, and decreased plasma LH, FSH, and testosterone levels, and although vitamin E is more effective than melatonin in preventing this damage, both are effective.

Effects of larazotide acetate, a tight junction regulator, on the liver and intestinal damage in acute liver failure in rats.

BACKGROUND AND AIM: The epithelial cells are the strongest determinants of the physical intestinal barrier. Tight junctions (TJs) hold the epithelial cells together and allow for selective paracellular permeability. Larazotide acetate (LA) is a synthetic octapeptide that reduces TJ permeability by blocking zonulin receptors. In this study, we aimed to investigate the effects of LA, a TJ regulator, on the liver and intestinal histology in the model of acute liver failure (ALF) in rats. MATERIALS AND METHODS: The thioacetamide (TAA) group received intraperitoneal (ip) injections of 300 mg/kg TAA for 3 days. The TAA+LA(dw) (drinking water) group received prophylactic 0.01 mg/mL LA orally for 7 days before the first dose of TAA. The LA(dw) group received 0.01 mg/mL LA orally. The TAA + LA(g) (gavage) group received prophylactic 0.01 mg/mL LA via oral gavage for 7 days before the first dose of TAA. The LA(g) group received 0.01 mg/mL LA via oral gavage. While liver tissue was evaluated only with light microscopy, intestinal samples were examined with light and electron microscopy. RESULTS: Serum ammonia, AST, and ALT levels in the TAA group were significantly higher than in control groups (all p < 0.01). Serum ALT levels in the TAA + LA(dw) group were significantly lower than in the TAA group (p < 0.05). However, serum ammonia and ALT levels did not differ between the TAA and other groups. Serious liver damage in the TAA group was accompanied by marked intestinal damage. There was no significant difference between the TAA and TAA + LA(dw) groups and TAA and TAA + LA(g) groups for liver damage scores. However, intestinal damage scores significantly decreased in the TAA + LA(dw) group compared to the TAA group. In the TAA + LA(dw) group, fusion occurred between the surface epithelial cells of neighboring villi and connecting regions formed as epithelial bridges between the villi. CONCLUSION: Our findings suggest that LA reduced intestinal damage by acting on TJs in the TAA-induced ALF model in rats.

Ameliorative effects of crocin on the inflammation and oxidative stress-induced kidney damages by experimental periodontitis in rat.

OBJECTIVES: The present study aimed to investigate the effects of periodontitis on kidneys and the protective role of crocin in periodontitis-induced kidney damage. MATERIALS AND METHODS: Ethics committee approval was obtained and 30 Wistar rats were randomly divided into 3 groups of 10 rats: Control (C), Periodontitis (P), and Periodontitis + Crocin (P + Cr). After the treatments, rat kidney tissues were incised under anesthesia and blood samples were collected. Biochemical and histopathological analyses were conducted on the samples. RESULTS: Malondialdehyde (MDA), total oxidant status (TOS), and oxidative stress index (OSI) increased in P group rat kidney tissues; urea, creatinine, Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin 1ß (IL-1ß) levels increased in the serum; glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and total antioxidant status (TAS) levels were reduced in rat kidney tissues, and renal histopathology deteriorated. In the P + Cr group, we observed improvements in biochemical and histopathological parameters when compared with the P group. CONCLUSION: Periodontitis (P) led to deterioration in oxidative stress parameters and histopathology by increasing the oxidants in kidney tissue. P also led to inflammation in the blood of the rats. Periodontitis + Crocin (P + Cr) administration alleviated the effects of P due to powerful antioxidant anti-inflammatory properties. Cr could be employed as a protective agent in P-induced inflammation and oxidative damage.

Protective effects of crocin on acrylamide-induced testis damage.

Exposure to acrylamide (Ac) through food is almost inevitable and this kind of toxicity may cause lifelong harm. In present study, we researched effects of Crocin (Cr) on testis histopathology in Ac-induced testis of rats. Adult male rats were grouped as: group 1, 1 ml saline only; group 2, 50 mg/kg Cr only; group 3, 25 mg/kg Ac only and group 4, 25 mg/kg Ac + 50 mg/kg Cr. All administrations were given as 1 ml/day by gavage for 21 days. It was found that Ac adversely influenced the levels of FSH, testosterone and LH in the blood serum; malondialdehyde (MDA), total antioxidant status (TOS), oxidative stress index (OSI)/ glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), total antioxidant status (TAS) oxidant/antioxidant parameters in testis tissue (p < .01) and the histopathological parameters like Johnson's score, seminiferous tubule diameter, seminiferous epithelial height and H-score for caspase-3 immunoreactivity. In contrary, Cr treatment resulted in increase in testosterone, follicle stimulating hormone (FSH), luteinizan hormone (LH) levels and SOD, CAT, GSH, TAS levels (p < .01) and improved all the histopathological changes. In conclusion, Cr has a promising protective potential against Ac-caused toxic damages in testicular tissue.

Glial Cell Line-Derived Neurotrophic Factor, S-100 Protein and Synaptophysin Expression in Biliary Atresia Gallbladder Tissue.

PURPOSE: Biliary atresia (BA) is a disease that manifests as jaundice after birth and leads to progressive destruction of the ductal system in the liver. The aim of this study was to investigate histopathological changes and immunohistochemically examine the expression of glial cell line-derived neurotrophic factor (GDNF), synaptophysin, and S-100 protein in the gallbladder of BA patients. METHODS: The study included a BA group of 29 patients and a control group of 41 children with cholecystectomy. Gallbladder tissue removed during surgery was obtained and examined immunohistochemically and histopathologically. Tissue samples of both groups were immunohistochemically assessed in terms of GDNF, S-100 protein, and synaptophysin expression. Expression was classified as present or absent. Inflammatory activity assessment with hematoxylin and eosin staining and fibrosis assessment with Masson's trichrome staining were performed for tissue sample sections of both groups. RESULTS: Ganglion cells were not present in gallbladder tissue samples of the BA group. Immunohistochemically, GDNF, synaptophysin, and S-100 expression was not detected in the BA group. Histopathological examination revealed more frequent fibrosis and slightly higher inflammatory activity in the BA than in the control group. CONCLUSION: We speculate that GDNF expression will no longer continue in this region, when the damage caused by inflammation of the extrahepatic bile ducts reaches a critical threshold. The study's findings may represent a missing link in the chain of events forming the etiology of BA and may be helpful in its diagnosis.

Is Decorin a Promising New Agent for Facial Nerve Regeneration? An Experimental Study.

OBJECTIVE: The aim of this study was to investigate the effects of systemic administration of decorin (DC) on facial nerve (FN) regeneration. METHODS: A total of 32 female albino Wistar rats were divided into 4 groups: control (C) group: no bilateral FN neurorrhaphy (B-FNN), no DC application, sham-operated group: B-FNN without DC application, DC group: DC application without B-FNN, and B-FNN + DC group: B-FNN and DC application. Nerve conduction studies were performed before and after skin incisions at 1st, 3rd, 5th, and 7th weeks in all groups. The amplitude and latency of compound muscle action potentials were recorded. FN samples were obtained and were investigated under light microscopy and immunohistochemical staining. The nerve and axon diameter, number of axons, H score, Schwann cell proliferation, and myelin and axonal degeneration were recorded quantitatively. RESULTS: In the sham group, the 3rd and 5th postoperative week, amplitude values were significantly lower than those of the B-FNN + DC group (p < 0.05). Nerve diameters were found to be significantly larger in the sham, DC, and B-FNN + DC groups than in the C group (p < 0.05). The number of axons, the axon diameter, and the H scores were found to be significantly higher in the B-FNN + DC group than in the sham group (p < 0.05). The Schwann cell proliferation, myelin degeneration, and axonal degeneration scores were significantly lower in the B-FNN + DC group than in the sham group (p < 0.05). CONCLUSION: Electrophysiological and histopathological evaluation revealed the potential benefits provided by DC. This agent may increase FN regeneration.

Impaction of the polylactic membrane or hydrofiber with silver dressings on the interleukin-6, tumor necrosis factor-α, transforming growth factor-b3 levels in the blood and tissues of pediatric patients with burns.

BACKGROUND: We aimed to evaluate the effects of two different burn dressings, hydrofiber with a silver (HFAg) and polylactic membrane (PLM), on altering the levels of important biomarkers Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α), Transforming growth factor-ß3 (TGF-ß3) in blood and burnt tissue in children with second-degree burns. METHODS: Children between the ages of one to 16 years, with 25-50% second-degree partial-thickness burns of the total body surface area were included in this study. Patients in the PLM group were dressed with PLM in a typical way according to the manual. The HFAg group was dressed with HFAg and a sterile cover. During and at the end of the 21-day treatment, blood and skin tissue samples were taken from the two burn and control groups. IL-6, TNF-α, and TGF-ß ß3 levels were evaluated in blood and tissue samples from all groups, and the results were analyzed statistically. RESULTS: In the PLM group, IL-6 and TNF-α levels decreased early days in both serum and tissue samples to reach normal ranges compared with the HFAg group. In the PLM group, TGF-ß3 levels were elevated than in other groups for two weeks. CONCLUSION: In this study, we found that PLM controls inflammation earlier in both systemic and burn tissue. We also found that PLM increased the level of TGF-ß3, which may be associated with the prevention of the development of hypertrophic scar in the burn wound, in the blood and burn tissue during this study.

Comparison of polycaprolactone and calcium hydroxylapatite dermal fillers in a rat model.

Polycaprolactone (PCL) and calcium hydroxylapatite (CaHA) are semipermanent dermal fillers that are frequently preferred in the last decade. This study aims to compare the effects of these two fillers in the rat skin. A total of 30 female rats were divided into; control, PCL, and CaHA group. Tissue samples taken at the second and fourth month were stained with hematoxylin-eosin, Masson trichrome, collagen type 1, and 3 immunohistochemical antibodies. Collagen density was quantitatively compared using the Image J computer program. At 2 and 4 months, the density of collagen increased in both filler groups compared to the control group. There was no significant difference between collagen density or type 1 and type 3 collagen H scores in the filler groups. The number of fibroblast nuclei was significantly higher in the PCL group at 4 months compared to the other two groups. Dermis thickness was found to be superior in both filler groups compared to the control group at the fourth month, there was no significant difference between the filler groups. We compared the effect of CaHA and PCL filler on collagenization histologically and immunohistochemically. We found that PCL and CaHA fillers are effective in increasing dermal collagen density, type 1 and type 3 collagen amount, and preventing dermis atrophy and showed that they have no advantage over each other in this respect. We have shown that PCL filler provides more fibroblast increase compared to CaHA filler and the effect of stimulating fibroblast proliferation takes longer.

Ameliorative effects of crocin on tartrazine dye-induced pancreatic adverse effects: a biochemical and histological study.

The present study aimed to analyze the impact of tartrazine (T) and crocin (Cr) applications on the pancreas tissues of the Wistar rats. A total of 40 Wistar rats were randomly divided into 4 groups with 10 rats in each group, including the Control, T, Cr, and T + Cr groups. After 3 weeks of application, the pancreatic tissues of the rats were removed under anesthesia and rat blood samples were obtained. Tissues were analyzed with biochemical and histopathological methods. It was determined that T administration increased malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), glucose, triglyceride, LDL, VLDL, and total cholesterol levels. However, it decreased reduced glutathione (GSH), total antioxidant status (TAS), superoxide dismutase (SOD), catalase (CAT), and HDL levels when compared with the other groups. It was observed that Cr administration significantly increased GSH, SOD, CAT, TAS, and HDL levels when compared with the control group. In the T group, histopathological changes were observed in pancreatic tissue, leading to damages in exocrine pancreas and islets of Langerhans and increased caspase-3 immunoreactivity (p ≤ 0.001). Co-administration of Cr and T brought the biochemical and histopathological findings closer to the control group levels. The administration of T induced damage in the pancreas with the administered dose and frequency. Cr can increase the antioxidant capacity in pancreas tissue. Co-administration of T and Cr contributed to the reduction of the toxic effects induced by T. It could be suggested that Cr administration ameliorated T toxicity.

Thymoquinone protection against 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin induced nephrotoxicity in rats.

We investigated the effects of thymoquinone (TQ) on kidney tissues of Wistar rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced nephrotoxicity. We used 50 rats divided into five groups; control, corn oil, TCDD, TQ, TCDD + TQ. We found that malondialdehyde (MDA), total oxidant status (TOS), blood urea nitrogen (BUN), creatinine, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) levels in the TCDD treated group increased significantly compared to the other groups, while reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and total antioxidant status (TAS) levels decreased in the TCDD group. In the TQ treated group, we found that GSH, SOD, CAT, TAS levels increased and MDA, TOS, IL-6 and TNF-α levels decreased compared to the other groups. The effects of TCDD on oxidative stress parameters, inflammatory markers and histological changes were ameliorated by TQ treatment.

A light microscopic investigation of the renoprotective effects of α-lipoic acid and α-tocopherol in an experimental diabetic rat model.

We investigated the effects of α-lipoic acid (AL) and α-tocopherol (AT) on renal histopathology in a streptozotocin (STZ) induced diabetic rat model. Adult male rats were divided into six groups: group 1, saline only; group 2, AL only; group 3, AT only; group 4, STZ only; group 5, STZ + AL; group 6 STZ + AT. Experimental diabetes was induced by STZ. AL and AT were administered for 15 days. Kidney sections were examined using a light microscope after hematoxylin and eosin (H & E), periodic acid-Schiff (PAS) and caspase-3 staining. Histological damage to glomeruli, tubule epithelial cells and basement membrane was observed in group 4. Administration of AT and AL reduced renal injury in the diabetic rats. Group 5 exhibited a greater curative effect on diabetic rats than group 6. AT and AL may be useful for preventing diabetic renal damage.

Protective effects of melatonin and vitamin E in acetamiprid-induced nephrotoxicity.

Investigation of probable toxic effects of acetamiprid (ACMP) on kidney and comparative analysis of the probable protective effects of vitamin E and melatonin were conducted in the present study. The ethics committee approval was obtained from Inonu University Medical Faculty Ethics Committee. Fifty Balb-c mice were randomly assigned to control, corn oil, ethyl alcohol, ACMP, ACMP + melatonin, ACMP + vitamin E, and ACMP + melatonin + vitamin E groups. At the end of the experiments, rat kidney tissues were incised under anesthesia. Blood samples and kidney tissues were examined. After 21 days of ACMP administration, it was observed that malondialdehyde (MDA), total oxidant status (TOS), BUN, creatinine, IL-6, IL-1ß, and TNF-α levels, histopathological damage, and Caspase-3 immunoreactivity scores increased, and glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and total antioxidant status (TAS) levels decreased, and histopathological damages were observed. Melatonin and vitamin E administration led to improvements in oxidative stress parameters, renal functions, inflammatory markers, and histopathological findings. ACMP administration led to nephrotoxicity in rat kidney tissues. Although melatonin and vitamin E administrations were effective on ACMP nephrotoxicity separately, co-administration of both was quite effective. Concomitant use of melatonin and vitamin E could be effective on prevention of toxicity.

Investigation of the cardiotoxic effects of parenteral nutrition in rabbits.

INTRODUCTION: Parenteral nutrition (PN) is used for the intravenous delivery of nutrients to patients who cannot take food orally. However, it is not clear whether PN also negatively impacts cardiac tissue. The present empirical study investigated the cardiac effects of PN in rabbits. METHODS: The effects of PN were examined in three groups of rabbits: animals in the PN + fasting group (n = 14) had been fully fasted before receiving a full PN dose via an intravenous central catheter; the PN + oral feeding group (n = 14) received half of the daily calorie requirement as a half dose of PN via an intravenous central catheter; the third group consisted of controls (n = 14) with full enteral feeding and full enteral fluid intake with no PN and no central venous catheter. At the end of the 10-day study period, the rabbits were subjected to echocardiographic examination and euthanized. Blood and tissue samples were obtained from all groups. DNA was isolated from nucleated blood cells. Tissue samples were examined by both light and electron microscopy, relative telomere length was determined from DNA, and blood samples were analyzed biochemically. RESULTS: At the end of the study, there were no statistically significant differences in weight change between the three groups. Echocardiography revealed minimally impaired diastolic function in the PN + fasting group compared to the other groups. Biochemical and histopathological analyses, relative telomere length determination, and electron micrographs showed significant cardiac damage in the PN + fasting group but not in the PN + oral feeding group or the control group. The blood biochemical analyses showed hyperglycemia and a low insulin level in the PN + fasting group but not in the other two groups. CONCLUSIONS: A combination of PN and fasting may damage the cardiac muscle cells of rabbits via a mechanism involving hyperglycemia and oxidative stress. Additional enteral feeding may protect against the destructive effects of PN on cardiac tissue.