Effect of Long-term Fluoride Exposure on Lipid Peroxidation and Histology of Testes in First- and Second-generation Rats

This experiment was designed to investigate the histological and lipid peroxidation effects of chronic fluorosis on testes tissues of first- and second-generation rats. Sixteen virgin female Wistar rats were mated with eight males (2:1) for approximately 12 h to obtain first-generation rats. Pregnant rats were divided into two groups: controls and fluoride-given group, each of which containing five rats. Pregnant rats in the fluoride-given group were exposed to a total dose of 30 mg/l sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/l of NaF throughout the gestation and lactation periods. After the lactation period, the young animals (first generation, F1) were exposed to the same dose of NaF in drinking water for 4 months. At the end of the 4 months of experimental period, nine randomly chosen male rats (F1) were killed and testes tissues were taken for histopathological and biochemical analysis. The remaining eight female rats were mated with four males (2:1) for approximately 12 h to obtain second-generation rats. Six female were identified as pregnant and treated with similarly throughout the gestation and the lactation periods. After the lactation period, the young male animals (second generation, F2) were also treated in the same way for 4 months. At the end of the 4 months of experimental period, nine randomly chosen male rats (F2) were killed and testes tissues were collected for histopathological and biochemical analysis. The rats in the control group were applied the same procedure without NaF administration. In biochemical analysis of the fluoride given F1 and F2 rats, it has been found that plasma fluoride levels and testes thiobarbituric acid reactive substance levels were significantly increased when compared with the control group. In F1 and F2 rats, similar histopathological changes were observed. In both groups, spermatogenesis was severely reduced. Spermatogonia and primary spermatocytes were normal, however, there was a widespread degeneration in other spermatogenic cell lines of the seminiferous epithelium. The histological structures of the Sertoli and interstitial Leydig cells were normally observed. It is concluded that chronic fluorosis exposure leads to a remarkable destruction in testes tissues of F1 and F2 rats via lipid peroxidation. The study was carried out in Suleyman Demirel University.     

The regulatory effect of melatonin on physiological,biochemical and molecular parameters in cold-stressed wheat seedlings

We investigated the possible mediatory role of melatonin in protecting wheat plants from cold stress. Ten-day-old wheat seedlings were pretreated with 1 mmol l^?1 melatonin for 12 h and subsequently exposed to stress conditions at 5/2 °C (day/night) for 3 days. Cold stress caused serious reductions in leaf surface area, water content, and photosynthetic pigment content, whereas melatonin application attenuated these reductions. Accumulation of reactive oxygen species (ROS), including superoxide and hydrogen peroxide, was very high in cold-stressed plants and caused lipid peroxidation in membranes. Concomitantly, ROS damaged the DNA profile and negatively influenced expression and/or activity of many enzymes, including RuBisCo. When compared to controls, cold-stressed plants had higher activities of the antioxidant enzymes superoxide dismutase, guaicol peroxidase, ascorbate peroxidase, and glutathione reductase and higher levels of the antioxidant compounds total ascorbate, reduced ascorbate, total glutathione, reduced glutathione, and phenolic substances; however, this elevation could not cope with the destructive effects of cold stress. Melatonin-pretreated plants exhibited greater increases in these parameters comparison with untreated cold-stressed plants. Isozyme bands monitored in native gel and RuBisCo expression supported these changes. Also, due to the cold-induced increase in dehydroascorbate and oxidized glutathione, the corrupted redox status in the cell was ameliorated by melatonin application. Similarly, levels of the osmoprotectants total soluble protein, carbohydrate, and proline were also increased by cold stress; however, melatonin-applied seedlings had a higher content of these solutes in comparison to untreated cold-stressed plants. We suggest that melatonin can improve plant resistance to cold stress in wheat seedlings by directly scavenging ROS and by modulating redox balance and other defence mechanisms.     

The human socio-cognitive niche and its evolutionary origins

Hominin evolution took a remarkable pathway, as the foraging strategy extended to large mammalian prey already hunted by a guild of specialist carnivores. How was this possible for a moderately sized ape lacking the formidable anatomical adaptations of these competing 'professional hunters'? The long-standing answer that this was achieved through the elaboration of a new 'cognitive niche' reliant on intelligence and technology is compelling, yet insufficient. Here we present evidence from a diversity of sources supporting the hypothesis that a fuller answer lies in the evolution of a new socio-cognitive niche, the principal components of which include forms of cooperation, egalitarianism, mindreading (also known as 'theory of mind'), language and cultural transmission, that go far beyond the most comparable phenomena in other primates. This cognitive and behavioural complex allows a human hunter-gatherer band to function as a unique and highly competitive predatory organism. Each of these core components of the socio-cognitive niche is distinctive to humans, but primate research has increasingly identified related capacities that permit inferences about significant ancestral cognitive foundations to the five pillars of the human social cognitive niche listed earlier. The principal focus of the present study was to review and integrate this range of recent comparative discoveries.     

Cycloartane-type glycosides from Astragalus schottianus

Three new cycloartane-type triterpene glycosides were isolated from the roots of Astragalus schottianus Boiss. Their structures were established as 20(R),25-epoxy-3-O-β-d-xylopyranosyl-24-O-β-d-glucopyranosyl-3β,6α,16β,24α-tetrahydroxycycloartane (1), 20(R),25-epoxy-3-O-[β-d-glucopyranosyl(1 → 2)]-β-d-xylopyranosyl-24-O-β-d-glucopyranosyl-3β,6α,16β,24α-tetrahydroxycycloartane (2), 3-O-β-d-xylopyranosyl-3β,6α,16β,20(S),24(S),25-hexahydroxycycloartane (3) by the extensive use of 1D and 2D-NMR techniques and mass spectrometry.     

The regulatory role of heparin on c-Met signaling in hepatocellular carcinoma cells

The role of heparin as an anticoagulant is well defined; however, its role in tumorigenesis and tumor progression is not clear yet. Some studies have shown that anticoagulant treatment in cancer patients improve overall survival, however, recent clinical trials have not shown a survival benefit in cancer patients receiving heparin treatment. In our previous studies we have shown the inhibitory effects of heparin on Hepatocyte Growth Factor (HGF)-induced invasion and migration in hepatocellular carcinoma (HCC) cells. In this study, we showed the differential effects of heparin on the behaviors of HCC cells based on the presence or absence of HGF. In the absence of HGF, heparin activated HGF/c-Met signaling and promoted motility and invasion in HCC cells. Heparin treatment led to c-Met receptor dimerization and activated c-Met signaling in an HGF independent manner. Heparin-induced c-Met activation increased migration and invasion through ERK1/2, early growth response factor 1 (EGR1) and Matrix Metalloproteinases (MMP) axis. Interestingly, heparin modestly decreased the proliferation of HCC cells by inhibiting activatory phosphorylation of Akt. The inhibition of c-Met signaling reversed heparin-induced increase in motility and invasion and, proliferation inhibition. Our study provides a new perspective into the role of heparin on c-Met signaling in HCC.     

Nitric oxide levels and antioxidant enzyme activities in jaundices of premature infants

Free radicals are effective in the genesis of several diseases in the neonatal period. This study aimed to show the relationship between serum bilirubin levels and plasma nitric oxide and the activity of enzymes in the erythrocyte such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in premature infants. In the study, 20 premature infants with newborn jaundice were included and the control group was formed by 15 premature infants without jaundice. Venous blood samples were taken from all neonates in the study and control groups on the first day of hospitalization. Plasma nitric oxide levels and activities of SOD, GSH-Px and CAT enzymes in the erythrocytes were investigated in these samples. Plasma nitric oxide and serum bilirubin levels were found to be significantly higher in the study group (47.4 +/- 7.25 micromol l(-1), 18.41 +/- 3.28 mg dl(-1), respectively) than those in the control group (33.46 +/- 6.43 micromol l(-1), 4.35 +/- 0.60 mg dl(-1), respectively; p < 0.001). In addition, erythrocyte SOD, GSH-Px and CAT enzyme activities (724 +/- 78.61, 673 +/- 90.5, 63 +/- 12.8 U g(-1) Hb, respectively) were found to be significantly lower in the study group than those in the control group (1208 +/- 129.04, 1097.6 +/- 75.8, 99.06 +/- 12.4 U g(-1) Hb, respectively, p < 0.001). It was concluded that in the aetiology of hyperbilirubinemia, neonatal erythrocytes and nitric oxide reactions are affected differently and that erythrocyte haemolysis caused as a result of these effects may play a role in the aetiopathogenesis of unconjugated hyperbilirubinemia. Haemolysis may also be seen because of the inadequacy of the protection by erythrocytes against the cytotoxic effects of free radicals resulting from the lack of antioxidant enzymes in these cells.