The Ability of Green Tea (Camellia sinensis) Extract in Modulating the Cytogenetic and Haematological Effects of Mitomycin C in Albino Male Mice

The present study aimed to investigate the toxic and mutagenic and anti – mutagenic effects of the aqueous extract (5, 10 and 15 mg/kg) of green tea (Camellia sinensis) in modulating the genotoxic effects of mitomycin C (MMC). Albino male mice (Mus musculs) were employed as a biological system and four parameters were performed in vivo; total leucocyte count, mitotic index, chromosomal aberrations and micronucleus formation. The plant extract was evaluated through three types of treatments. In the first, the extract was given alone orally. While the second and third treatment included two types of interactions with MMC; pre – and post – MMC treatments. All treatments were paralleled by negative and positive controls. In the first treatment, the dose 15 mg/kg of green tea extract enhanced the parameters investigated and a significant increase was observed in total count of leucocyte (8070 cells/cu. mm. blood) as compared to either negative (6900 cells/cu. mm. blood) or positive (5060 cells/cu. mm. blood) controls, Such observation was positively correlated with the mitotic index. In contrast, the spontaneous formation of micronuceli and chromosomal aberrations were decreased in the three investigated doses of the extract. The results showed that the plant extract had no genotoxic or mutgenic effects. In the second and third treatments, green tea extract showed a good performance in protecting the bone marrow cells in mice against genotoxic MMC effect by increasing the total leucocyte count and mitotic index and decreasing the chromosomal aberration and mironuclei when the treatment were before or after the MMC

Hypoxia-Modified Cancer Cell Metabolism

While oxygen is critical to the continued existence of complex organisms, extreme levels of oxygen within a system, known as hypoxia (low levels of oxygen) and hyperoxia (excessive levels of oxygen), potentially promote stress within a defined biological environment. The consequences of tissue hypoxia, a result of a defective oxygen supply, vary in response to the gravity, extent and environment of the malfunction. Persistent pathological hypoxia is incompatible with normal biological functions, and as a result, multicellular organisms have been compelled to develop both organism-wide and cellular-level hypoxia solutions. Both direct, including oxidative phosphorylation down-regulation and inhibition of fatty-acid desaturation, and indirect processes, including altered hypoxia-sensitive transcription factor expression, facilitate the metabolic modifications that occur in response to hypoxia. Due to the dysfunctional vasculature associated with large areas of some cancers, sections of these tumors continue to develop in hypoxic environments. Crucial to drug development, a robust understanding of the significance of these metabolism changes will facilitate our understanding of cancer cell survival. This review defines our current knowledge base of several of the hypoxia-instigated modifications in cancer cell metabolism and exemplifies the correlation between metabolic change and its support of the hypoxic-adapted malignancy

Epigenetics in Male Infertility

Male infertility is a complex medical condition, in which epigenetic factors play an important role. Epigenetics has recently gained significant scientific attention since it has added a new dimension to genomic and proteomic research. As a mechanism for maintaining genomic integrity and controlling gene expression, epigenetic modifications hold a great promise in capturing the subtle, yet very important, regulatory elements that might drive normal and abnormal sperm functions. The sperm’s epigenome is known to be marked by constant changing over spermatogenesis, which is highly susceptible to be influenced by a wide spectrum of environmental stimuli. Recently, epigenetic aberrations have been recognized as one of the causes of idiopathic male infertility. Recent advances in technology have enabled humans to study epigenetics role in male infertility