The paper reviews the aspects of physiology and biochemistry of microbial biodegradation of the main components of petroleum oil: alkanes (larger than methane), alkenes, alkines, cyclic, polycyclic, aromatic and polyaromatic hydrocarbons. It focuses on aerobic degradation pathways. The review provides key information prepared on the basis of more than 30 years of research on microbial degradation of hydrocarbons. The areas discussed include new pathways of biodegradation of branched-chain alkanes, cyclic and polyaromatic hydrocarbons which have been discovered during the past few years. Special attention was paid to oxygenases ? enzymes initiating aerobic metabolism of hydrocarbons and phenomenon of co-oxidation which enables assimilation of most recalcitrant components of crude oil.
In this paper we have presented data on an environmental exposure to N-nitrosodimethylamine (NDMA) and factors which favour endogenoeaus biosynthesis of this compound. The factors influencing metabolism and toxicity as well as health effect of exposure have been reported.
Phosphodiesterases of cyclic nucleotides (PDEs) are enzymes hydrolyzing cGMP, cAMP or both and are regulated in several different ways. In this paper we summarize current data on structure, cellular and tissue localization, regulation and function of different PDE families that hydrolyze cGMP.
Neurotensin is a 13-amino acid hormonal peptide which was first isolated from bovine hypothalamus. It is present in the digestive tract as well as in the central nervous system. It has a variety of biological activities as a central neurotransmitter or neuromodulator, and a peripheral hormone. NT receptors have been characterized in a variety of tissues and cell lines of peripheral and central organs. The physiological functions of NT include stimulation of pancreatic and biliary secretion, stimulation of colonic motility, inhibition of small bowel and gastric motility, trophic effect on numerous tissues of the gastrointestinal tract. NT exerts hypothermic and analgesis effect when injected into the central nervous system. From a clinical standpoint, studies with NT have led to implications of its involvment in schizophrenia, Parkinson's disease and Alzheimer's disease.
The phenylpropanoid metabolism in plants is an important source of numerous compounds of great importance in development and defense. In particular, flavonoids play a significant role as signal compounds, phytoalexins, UV-protectants, pigments etc. Numerous enzymes (PAL, CHS, CHI, CHR, IFR and many others) are involved in this branched metabolic pathway. The key enzymes of phenylpropanoid biosynthesis are phenylalanine ammonia-lyase (PAL), and chalcone synthase (CHS). Both enzymes (as well as some other of the pathway) are encoded by multigene families. The organospecific expression of different members of these families is presumably the key factor for the regulation of the entire pathway. Several cis-elements, and trans-acting factors have been already described, however it is too early to formulate the conclusive model of the overall transcriptional regulation of the phenylpropanoid metabolism.
In 1994, Kuhajda and colleagues unambiguously identified the oncogenic antigen-519, a prognostic molecule found in breast cancer patients with markedly worsened prognosis, as fatty acid synthase (FAS), the key enzyme for the de novo fatty acid biosynthesis. It now appears that human carcinomas and their pre-neoplastic lesions constitutively overexpress FAS and undergo significant endogenous fatty acid biosynthesis. Moreover, FAS blockade specifically induces apoptotic cancer cell death and prolongs survival of cancer xenograft hosts. Therefore, FAS signaling seems to play a central role in the maintenance of the malignant phenotype by enhancing cancer cell survival and proliferation. This review documents the rapidly changing perspectives on the function of FAS in cancer biology. First, we describe molecular mechanism by which aberrant transduction cascades driven by oncogenic changes subvert the down-regulatory effects of dietary fatty acids, resulting in tumor-associated FAS insensitivity to nutritional signals. Second, we speculate on the putative function that hypoxia can play as the epigenetic factor that triggers and maintains FAS overexpression in cancer cells by inducing changes in gene expression and in metabolism for survival. Third, we explore the role that FAS exhibits in cancer evolution by specifically regulating cancer-related proteins such as Her-2/neu oncogene and estrogen receptor. Finally, we reveal previously unrecognized functions of FAS on the response of cancer cells to chemo-, endocrine-, and immuno-therapies. These findings, all together, should ultimately enhance our understanding of how FAS-dependent endogenous fatty acid metabolism, once considered a minor anabolic-energy-storage pathway in normal cells, has become a jack-of-all-trades in cancer cells.
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