16 research outputs found
Radiations and male fertility
During recent years, an increasing percentage of male infertility has to be attributed to an array of environmental,
health and lifestyle factors. Male infertility is likely to be affected by the intense exposure to heat and extreme
exposure to pesticides, radiations, radioactivity and other hazardous substances. We are surrounded by several types
of ionizing and non-ionizing radiations and both have recognized causative effects on spermatogenesis. Since it is
impossible to cover all types of radiation sources and their biological effects under a single title, this review is
focusing on radiation deriving from cell phones, laptops, Wi-Fi and microwave ovens, as these are the most
common sources of non-ionizing radiations, which may contribute to the cause of infertility by exploring the effect
of exposure to radiofrequency radiations on the male fertility pattern. From currently available studies it is clear that
radiofrequency electromagnetic fields (RF-EMF) have deleterious effects on sperm parameters (like sperm count,
morphology, motility), affects the role of kinases in cellular metabolism and the endocrine system, and produces
genotoxicity, genomic instability and oxidative stress. This is followed with protective measures for these radiations
and future recommendations. The study concludes that the RF-EMF may induce oxidative stress with an increased
level of reactive oxygen species, which may lead to infertility. This has been concluded based on available
evidences from in vitro and in vivo studies suggesting that RF-EMF exposure negatively affects sperm quality
Pitfalls when examining gap junction hemichannels: interference from volume-regulated anion channels
Sphingosine 1-Phosphate Activation of EGFR As a Novel Target for Meningitic Escherichia coli Penetration of the Blood-Brain Barrier
Central nervous system (CNS) infection continues to be an important cause of mortality and morbidity, necessitating new approaches for investigating its pathogenesis, prevention and therapy. Escherichia coli is the most common Gram-negative bacillary organism causing meningitis, which develops following penetration of the blood-brain barrier (BBB). By chemical library screening, we identified epidermal growth factor receptor (EGFR) as a contributor to E. coli invasion of the BBB in vitro. Here, we obtained the direct evidence that CNS-infecting E. coli exploited sphingosine 1-phosphate (S1P) for EGFR activation in penetration of the BBB in vitro and in vivo. We found that S1P was upstream of EGFR and participated in EGFR activation through S1P receptor as well as through S1P-mediated up-regulation of EGFR-related ligand HB-EGF, and blockade of S1P function through targeting sphingosine kinase and S1P receptor inhibited EGFR activation, and also E. coli invasion of the BBB. We further found that both S1P and EGFR activations occurred in response to the same E. coli proteins (OmpA, FimH, NlpI), and that S1P and EGFR promoted E. coli invasion of the BBB by activating the downstream c-Src. These findings indicate that S1P and EGFR represent the novel host targets for meningitic E. coli penetration of the BBB, and counteracting such targets provide a novel approach for controlling E. coli meningitis in the era of increasing resistance to conventional antibiotics