Sphingosine kinase inhibitor, SKI-II confers protection against the ionizing radiation by maintaining redox homeostasis most likely through Nrf2 signaling.

Exposure to ionizing radiation (IR) set a series of deleterious events causing acute radiation syndrome and mortality, posing the need for a potent and safe radio-protective drug. IR induces cell death predominantly by causing oxidative stress and macromolecular damage. The pre-existing antioxidant defence machinery of the cellular system plays a crucial role in protecting the cells against oxidative stress by activation of Nrf2.

3,4-Dimethoxyphenyl bis-benzimidazole derivative, mitigates radiation-induced DNA damage.

Radiation-induced DNA damage initiates a series of overlapping responses that include DNA damage recognition and repair, induction of cell cycle checkpoints, senescence and/or apoptosis. This study assessed the DNA damage response and whole genome expression profile in two mammalian cell lines (HEK and U87) in response to (5-{4-methylpiperazin-1-yl}-2-[2'-(3,4-dimethoxyphenyl)-5'-benzimidazolyl] benzimidazole) DMA and ionizing radiation. DMA has been shown to act as a potent radiation protector, yielding significant levels of protection, i.

Sex-dependent effects of the UCP1 -3826 A/G polymorphism on obesity and blood pressure.

Objective: To ascertain the association of -3826 A/G polymorphism with blood pressure and different obesity markers.

Design And Subjects: A total of 96 adult participants (49 males, 47 females) were studied. Anthropometric measurements and blood pressure were taken using standardized techniques.

Characterization of nuclear glutamate dehydrogenase of chicken liver and brain.

Glutamate dehydrogenase (GDH) enzyme is recently being reported to be present in the nucleus in addition to the mitochondria in a number of organisms. Here we investigated the distribution of GDH in liver and brain tissues of chicken. Polyclonal anti-GDH antibody against bovine GDH was raised by us, which was later shown to be immunereactive to chicken GDH.

Bacterial endotoxin (LPS)-induced DNA damage in preimplanting embryonic and uterine cells inhibits implantation.

Objective: To investigate lipopolysaccharide (LPS)-induced DNA damage in preimplanting embryonic and uterine cells during preimplantation period of pregnancy that may ultimately inhibit the process of implantation in mouse.

Design: Animal study.

Setting: Academic research environment.

Role of tumor necrosis factor-α in Gram-negative bacterial lipopolysaccharides induced implantation failure.

Gram-negative bacterial lipopolysaccharides (LPS) are known causative agents for pregnancy loss in mothers with genital tract infections. In this study, we attempt to test the role of tumor necrosis factor-α (TNF-α) in the normal physiological processes of preimplantation embryonic development and LPS induced pregnancy loss in mice. Since the preimplantation mouse embryos grow in an unattached state for a considerable period (day 1-4.

Comprehending the role of LPS in Gram-negative bacterial vaginosis: ogling into the causes of unfulfilled child-wish.

Introduction: Intrauterine infection is frequently associated with pregnancy loss in pregnant women.

Discussion: This article reviews the role of Gram-negative bacterial infection in various complications related to early pregnancy and subsequent pregnancy loss. Here we discuss the pathways of ascending intrauterine infection, microbiology and the pathophysiology of such infections.