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Organic Synthesis at VWR VWR has All You Need for Organic Synthesis

Other exposures may induce the synthesis of a protective protein in the body. The best example is probably metallothionein, which binds cadmium and promotes the excretion of this metal; cadmium exposure is one of the factors that result in increased expression of the metallothionein gene. Similar protective proteins may exist but have not yet been explored sufficiently to become accepted as biomarkers. Among the candidates for possible use as biomarkers are the so-called stress proteins, originally referred to as heat shock proteins. These proteins are generated by a range of different organisms in response to a variety of adverse exposures.

(1984) Regulation of biosynthesis of ergot alkaloids by  Penicillium sizovae.

The section then provides two general overviews on toxicology at the mechanistic level. Mechanistically, modern toxicologists consider that all toxic effects manifest their first actions at the cellular level; thus, cellular responses represent the earliest indications of the body’s encounters with a toxic agent. It is further assumed that these responses represent a spectrum of events, from injury through death. Cell injury refers to specific processes utilized by cells, the smallest unit of biological organization within organs, to respond to challenge. These responses involve changes in the function of processes within the cell, including the membrane and its ability to take up, release or exclude substances; the directed synthesis of proteins from amino acids; and the turnover of cell components. These responses may be common to all injured cells, or they may be specific to certain types of cells within certain organ systems. Cell death is the destruction of cells within an organ system, as a consequence of irreversible or uncompensated cell injury. Toxic agents may cause cell death acutely because of certain actions such as poisoning oxygen transfer, or cell death may be the consequence of chronic intoxication. Cell death can be followed by replacement in some but not all organ systems, but in some conditions cell proliferation induced by cell death may be considered a toxic response. Even in the absence of cell death, repeated cell injury may induce stress within organs that compromises their function and affects their progeny.

Curcumin | Linus Pauling Institute | Oregon State …

III.2.2 Biosynthesis The ergoline ring system in ergot fungi is built up from L-tryptophan and mevalonic acid (Fig.

Dietary habits have an important influence on susceptibility to chemical toxicity, mostly because adequate nutrition is essential for the functioning of the body’s chemical defence system in maintaining good health. Adequate intake of essential metals (including metalloids) and proteins, especially the sulphur-containing amino acids, is necessary for the biosynthesis of various detoxificating enzymes and the provision of glycine and glutathione for conjugation reactions with endogenous and exogenous compounds. Lipids, especially phospholipids, and lipotropes (methyl group donors) are necessary for the synthesis of biological membranes. Carbohydrates provide the energy required for various detoxification processes and provide glucuronic acid for conjugation of toxic chemicals and their metabolites. Selenium (an essential metalloid), glutathione, and vitamins such as vitamin C (water soluble), vitamin E and vitamin A (lipid soluble), have an important role as antioxidants (e.g., in controlling lipid peroxidation and maintaining integrity of cellular membranes) and free-radical scavengers for protection against toxic chemicals.

I.4.2.5 Biochemical effects and mode of action Ochratoxin A is an inhibitor of tRNA synthetase and protein synthesis in several microorganisms ( Bacillus subtilis, B.

Salicylic acid (PIM 642) - INCHEM

1), and classified according to biosynthetic origin as pentaketides within the group of polyketides (Turner, 1971).

Platelets are especially susceptible to this action as they are incapable of regenerating the enzyme, presumably they have little or no capacity for protein biosynthesis (Brantmark et al., 1981).

TRICHOTHECENES II.1 Properties and analytical methods II.1.1 Physical and chemical properties II.1.1.1 Physical properties II.1.1.2 Chemical properties II.1.2 Analytical methods for trichothecenes II.1.2.1 Chemical methods II.1.2.2 Immunological methods II.1.2.3 Biological methods II.2 Sources and occurrence II.2.1 Taxonomic considerations II.2.2 Ecology of trichothecene-producing fungi II.2.3 Natural occurrence II.2.3.1 Agricultural products II.2.3.2 Trichothecenes in human foodstuffs II.3 Metabolism II.3.1 Absorption and tissue distribution II.3.1.1 Animal studies II.3.2 Metabolic transformation II.3.3 Excretion II.3.3.1 Animal studies II.3.3.2 Excretion in eggs and milk II.4 Effects on animals II.4.1 Field observations II.4.2 Effects on experimental animals II.4.2.1 General toxic effects II.4.2.2 Haematological and haemostatic changes II.4.2.3 Disturbances of the central nervous system II.4.2.4 Dermal toxicity II.4.2.5 Impairment of immune response II.4.2.6 Carcinogenicity II.4.2.7 Mutagenicity II.4.2.8 Teratogenicity and reproductive effects II.4.3 Biochemical effects and mode of action II.4.3.1 Cytotoxicity II.4.3.2 Inhibition of protein synthesis II.4.3.3 Inhibition of nucleic acid synthesis II.4.3.4 Alterations of cellular membranes II.4.3.5 Other biochemical effects II.4.4 Structure-activity relationships II.4.5 Prevention and therapy of trichothecene toxicosis II.5 Effects on man II.5.1 Contemporary episodes of human disease II.5.2 Historical Fusarium-related diseases II.5.3 Skin irritation II.5.4 Studies of haemostasis II.5.5 Airborne trichothecene-related diseases II.5.6 Toxicological information on man, obtained from therapeutic uses II.6 Evaluation of the human health risksIII.

(1978) Genetic and biochemical characterization of mutants of CHO cells resistant to the protein synthesis inhibitor trichodermin.
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Methotrexate 25 mg/ml solution for injection - - (eMC)

Recently, we divided the mammalian P450 gene superfamily into three groups (Nebert and McKinnon 1994)—those involved principally with foreign chemical metabolism, those involved in the synthesis of various steroid hormones, and those participating in other important endogenous functions. It is the xenobiotic-metabolizing P450 enzymes that assume the most significance for prediction of toxicity.

Chapter 33 - Toxicology INTRODUCTION

Given the apparent lack of physiological substrates, it is possible that P450 enzymes in families CYP1, CYP2, CYP3 and CYP4 that have appeared in the past several hundred million years have evolved as a means of detoxifying foreign chemicals encountered in the environment and diet. Clearly, evolution of the xenobiotic-metabolizing P450s would have occurred over a time period which far precedes the synthesis of most of the synthetic chemicals to which humans are now exposed. The genes in these four gene families may have evolved and diverged in animals due to their exposure to plant metabolites during the last 1.2 billion years—a process descriptively termed “animal-plant warfare” (Gonzalez and Nebert 1990). Animal-plant warfare is the phenomenon in which plants developed new chemicals (phytoalexins) as a defence mechanism in order to prevent ingestion by animals, and animals, in turn, responded by developing new P450 genes to accommodate the diversifying substrates. Providing further impetus to this proposal are the recently described examples of plant-insect and plant-fungus chemical warfare involving P450 detoxification of toxic substrates (Nebert 1994).

Methotrexate Injection - FDA prescribing information, …

Cancer mechanisms. Cancer is a multiplicity of diseases, and while the understanding of certain types of cancer is increasing rapidly due to the many molecular biological techniques that have been developed since 1980, there is still much to learn. However, it is clear that cancer development is a multi-stage process, and critical genes are key to different types of cancer. Alterations in DNA (somatic mutations) in a number of these critical genes can cause increased susceptibility or cancerous lesions (see “Genetic toxicology”). Exposure to natural chemicals (in cooked foods like beef and fish) or synthetic chemicals (like benzidine, used as a dye) or physical agents (ultraviolet light from the sun, radon from soil, gamma radiation from medical procedures or industrial activity) are all contributors to somatic gene mutations. However, there are natural and synthetic substances (such as anti-oxidants) and DNA repair processes which are protective and maintain homeostasis. It is clear that genetics is an important factor in cancer, since genetic disease syndromes such as xeroderma pigmentosum, where there is a lack of normal DNA repair, dramatically increase susceptibility to skin cancer from exposure to ultraviolet light from the sun.

Viral Infections of the Mouth: Overview, Human …

Animal studies have revealed that after penetration into the cell, some metal ions are bound to a specific protein, metallothionein. This low molecular weight protein is present in the cells of liver, kidney and other organs and tissues. Its sulphydryl groups can bind six ions per molecule. Increased presence of metal ions induces the biosynthesis of this protein. Ions of cadmium are the most potent inducer. Metallothionein serves also to maintain homeostasis of vital copper and zinc ions. Metallothionein can bind zinc, copper, cadmium, mercury, bismuth, gold, cobalt and other cations.

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