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AGENT (OXIDANT), OXIDATION, SUBSTRATE

(CHEMICAL), OXIDATION-REDUCTION REACTION.

Persistence The tendency of a compound (e.g., an insecticide) to resist degradation by biological means (e.g., metabolism by microorganisms) after that compound has been introduced into the environment (e.g., sprayed onto a field) or by physical means (degradation caused by exposure to sunlight, moisture, etc.). See also METABOLISM, MICRO-

ORGANISM, BIODEGRADABLE.

Pfiesteria piscicida A single-celled microscopic algae which has a predator/prey relationship with fish in its ecosystem. During a large portion of its life cycle, Pfiesteria piscicida exists in a nontoxic cyst form at the bottom of a river. When those (cysts) detect certain substances (e.g., excreta) emitted by live fish, the Pfiesteria piscicida transform into an amoeboid or dinoflagellate form, which secretes a water-soluble neurotoxin into the water (which incapacitates nearby fish). The Pfiesteria piscicida next attach themselves to those fish, and excrete a lipidsoluble toxin which destroys the epidermal layer of the fish’s skin, allowing the Pfiesteria piscicida to begin “eating” the fish’s tissue. Human exposure to the neurotoxin apparently causes short-term memory loss.

See also ECOLOGY, CELL, TOXIN, LIPIDS.

PPHA See POLYHYDROXYALKANOIC ACID (PHA).

Phage Abbreviation for bacteriophage. Another name for a specific type of virus. A virus that attacks bacteria is known as a bacteriophage. Bacteriophages are frequently used as vectors for carrying (foreign) DNA

into cells by genetic engineers. See also BAC-

TERIOPHAGE, VECTOR, GENETIC ENGINEERING,

TRANSFECTION, DEOXYRIBONUCLEIC ACID (DNA).

Phagocyte A cell such as a leukocyte that engulfs and digests cells, cell debris, microorganisms, and other foreign bodies in the bloodstream and tissues (phagocytosis). The ingested material is then degraded via enzymes. A whole class of cells is known to be phagocytic. See also MACROPHAGE,

MICROPHAGE, MONOCYTES, T CELLS, POLYMOR-

PHONUCLEAR LEUKOCYTES (PMN), CELLULAR

IMMUNE RESPONSE, POLYMORPHONUCLEAR GRAN-

ULOCYTES, LYSOSOME.

Pharmacoenvirogenetics A word coined during 2000 by Tim Studt to describe the fact that environmental factors interact with a given individual’s (human/animal/plant) genetic makeup (i.e., genome) to determine those individual’s (body’s) response to a given pharmaceutical (and/or progression of a disease). Those environmental factors include:

Foods eaten

The stress the individual is exposed to

Air and water pollution the individual is exposed to

Temperature and humidity the individual is exposed to

Geographical elevation the individual is exposed to

Bacteria the individual is exposed to

For example, when Rhizobium japonicum bacteria grow in the soil near the roots of a soybean plant (Glycine max L.), that causes certain specific genes in the soybean plant to be expressed (i.e., “turned on”) so that soybean plant’s roots become more hospitable as a “home” for those Rhizobium japonicum bacteria to live symbiotically (in nodules on the roots) with the soybean plant. See also

PHARMACOKINETICS, GENETICS, PHARMACOLOGY,

PHARMACOGENETICS, ABSORPTION, METABOLISM,

SNP, ALLELE, HAPLOTYPE, HAPTOGLOBIN, RHIZO-

BIUM (BACTERIA), NODULATION, SYMBIOTIC, CEN-

TRAL DOGMA (NEW), ACCLIMATIZATION.

Pharmacogenetics A branch of pharmacokinetics that deals with the reactions between drugs, or free radicals, or synthetic food ingredients, and specific individuals due to the genetics of those individuals. The subgroup of all those individuals whose DNA causes their bodies to respond in a specific way to a given drug or synthetic food ingredient, is known as a HAPLOTYPE. For example, one haplotype (subgroup) of pediatric leukemia patients suffers severe and life-threaten- ing reactions to some commonly used leukemia treatment drugs, due to the variation (i.e., SNP) in the thiopurine S-methyl transferase gene (allele) in their genome. Another example is that consumption of

© 2002 by CRC Press LLC

sodium-containing food ingredients tends to cause a dangerous increase in blood pressure (hypertension) among the African-American people living in the U.S., more often than among other ethnic groups living in the U.S.

See also PHARMACOKINETICS, PHARMACOGENOMICS, GENETICS, PHARMACOLOGY, ABSORPTION,

METABOLISM, HAPLOTYPE, DEOXYRIBONUCLEIC

ACID (DNA), MUTATION, SNP, ALLELE, CANCER,

HAPTOGLOBIN, TRANSVERSION.

Pharmacogenomics A branch of pharmacokinetics that deals with the biological impacts of pharmaceuticals or synthetic food ingredients, and the specific differences in response/reaction of living structures (tissues, organs, etc.) due to different genomes (DNA) of those individual organisms that consume those pharmaceuticals or food ingredients. The subgroup consisting of all those individuals whose genome (DNA) causes their body to respond in a specific way to a given pharmaceutical, free radical, or synthetic food ingredient, is known as a HAPLOTYPE. A haplotype could (theoretically) be as small as one individual (e.g., one woman, possessing an as yet unknown genome), because that woman’s particular specific response to a pharmaceutical could result from one single-nucleotide polymorphism (SNP) that only her genome possesses. Thus, pharmacogenomics is the pharmacokinetics (of a given pharmaceutical or food ingredient) within a specific haplotype.

For example, some ethnic minorities, genders, and individuals have far different biological reactions/responses to certain pharmaceuticals (e.g., the painkiller morphine works better in women, aspirin “thins” men’s blood better than women’s blood, the painkiller ibuprofen works better in men, the diuretic drug thiazide works to control hypertension in 60% of U.S. African Americans but only 8% of U.S. Caucasian people, etc.), and food ingredients (e.g., monosodium glutamate, lactase, ethanol, etc.) impact some members of some ethnic minorities more than they do the majority of humans. That is due to the fact that different gene(s) within their genomes (DNA) cause synthesis of certain different proteins (generally enzymes),

which thereby cause the tissues/bodies of those individuals/ethnic minorities to react differently to specific pharmaceuticals or food ingredients in terms of:

• Absorption — transport of the drug (pharmaceutical) or food ingredient into the bloodstream (e.g., from the intestinal tract, in the case of food ingredients or orally administered drugs).

• Distribution — initial physical disposition/behavior of the substance in the body after the substance enters the body tissues. For example, does the substance preferentially concentrate in the fat cells (adipose tissue) of the body, or in other specific tissues?

• Metabolism — breakdown of the substance (if breakdown does occur) into other chemical compounds, and the ultimate disposition in the body of those compounds (or the original substance, if breakdown does not occur).

• Elimination — the speed and thoroughness with which the substance is excreted or is otherwise removed from the body.

See also PHARMACOKINETICS, GENOMICS, PHAR-

 

MACOLOGY, ADME TESTS, ABSORPTION, METABO-

 

P

LISM, GENOME, DEOXYRIBONUCLEIC ACID (DNA),

 

DIGESTION (WITHIN ORGANISMS), PHASE I CLINI-

 

 

CAL TESTING, HAPLOTYPE, CONSENSUS SEQUENCE,

 

PHARMACOGENETICS, GENE, ALLELE, SINGLE-

 

NUCLEOTIDE POLYMORPHISMS (SNPs), PROTEIN,

 

ENZYME, HAPTOGLOBIN, ADIPOSE.

 

Pharmacokinetics (pharmacodynamics) A

 

branch of pharmacology dealing with the

 

reactions between drugs or synthetic food

 

ingredients and living structures (e.g., tis-

 

sues, organs). The study of the:

 

• Absorption — transport of the drug (pharmaceutical) or food ingredient into the bloodstream (e.g., from the intestinal tract, in the case of food ingredients).

• Distribution — initial physical disposition/behavior of the substance in the body after the substance enters the

© 2002 by CRC Press LLC

body. For example, does the substance preferentially concentrate in the fat cells of the body?

Metabolism — breakdown of the substance (if breakdown does occur) into other compounds, and ultimate disposition of those compounds (or the original substance, if breakdown does not occur). For example, some pharmaceuticals break down into smaller compound(s); one of which then acts upon the relevant body cells (to relieve pain, lower blood pressure, etc.).

Elimination — the speed and thoroughness with which the substance is excreted or otherwise removed from the body.

In short, pharmacokinetics deals with what happens to a substance that is introduced into a living system. For example, how quickly it is broken down, to what intermediates and metabolites it is broken down, and what the pathway of this breakdown is. See also PHAR-

MACOLOGY, ADME TESTS, ABSORPTION, METABO-

LISM, INTERMEDIARY METABOLISM, DIGESTION

(WITHIN ORGANISMS), PHASE I CLINICAL TESTING,

PHARMACOGENOMICS, PHARMACOGENETICS, PHAR-

MACOENVIROGENETICS, PATHWAY.

Pharmacology The study of chemicals (e.g.,

Ppharmaceuticals) and their effects on living

organisms. See also PHARMACOKINETICS,

PHARMACOGENOMICS, PHARMACOGENETICS.

Pharmacophore The portion of a molecule (e.g., a pharmaceutical) that is responsible for its biological activity (i.e., therapeutic action on recipient’s tissue, etc.). See also

BIOLOGICAL ACTIVITY, ACTIVE SITE, CATALYTIC

SITE, MINIPROTEINS.

Phase I Clinical Testing The first in a series of human tests of new pharmaceuticals, mandated by the U.S. Food and Drug Administration (FDA). The primary purpose of the Phase I clinical test is to detect if the new pharmaceutical is toxic or otherwise harmful to normal, healthy humans. The conclusion of Phase I testing leads to Phase II and Phase III testing.

During the 1990s, the FDA began to require the inclusion of ethnic minorities and women (in addition to men) as subjects in

these tests, to enable pharmacogenomics (i.e., the testing to determine if a given pharmaceutical causes nontypical response in the bodies of members of these subgroups). See

also FOOD AND DRUG ADMINISTRATION (FDA),

KEFAUVER RULE, KOSEISHO, BUNDESGESUNDHEIT-

SAMT (BGA), COMMITTEE FOR PROPRIETARY

MEDICINAL PRODUCTS (CPMP), IND, IND EXEMP-

TION, PHARMACOGENOMICS, HAPLOTYPE, PHASE II

CLINICAL TESTS.

Phase II Clinical Tests The second in a series of human tests of new pharmaceuticals, mandated by the U.S. Food and Drug Administration (FDA). The primary purpose of the Phase II clinical tests is to determine the pharmaceutical’s efficacy (i.e., does it work?). Successful conclusion of Phase II tests allows Phase III clinical tests to begin. See also PHASE

I CLINICAL TESTING, FOOD AND DRUG ADMINIS-

TRATION (FDA), KEFAUVER RULE, KOSEISHO,

BUNDESGESUNDHEITSAMT (BGA), COMMITTEE FOR

PROPRIETARY MEDICINAL PRODUCTS (CPMP), IND,

IND EXEMPTION.

Phase III Clinical Tests The third in a series of human tests of new phamaceuticals, mandated by the U.S. Food and Drug Administration (FDA). The primary purpose of Phase III clinical tests is to verify proper dosage of a new pharmaceutical. See also PHASE I CLIN-

ICAL TESTING, PHASE II CLINICAL TESTS, FOOD AND

DRUG ADMINISTRATION (FDA), KEFAUVER RULE,

KOSEISHO, BUNDESGESUNDHEITSAMT (BGA), COM-

MITTEE FOR PROPRIETARY MEDICINAL PRODUCTS

(CPMP).

PHB See POLYHYDROXYLBUTYLATE.

Phenolic Hormones A category of compounds found in the human body, that are synthesized (manufactured) by the body from certain phenolic dietary substances (phytochemicals) such as isoflavones. Research indicates that phenolic hormones act to prevent a number of cancers such as those of the prostate, breast, large bowel, etc.

See also HORMONE, PHYTOCHEMICALS, ISOFLAVONES, CANCER, SELECTIVE ESTROGEN EFFECT.

Phenomics Utilized to refer to the relationship between genomics and phenotype/traits. See

also FUNCTIONAL GENOMICS, PHENOTYPE, TRAIT,

GENE FUNCTION ANALYSIS.

Phenotype The outward appearance (structure) or other visible characteristics of an

© 2002 by CRC Press LLC

organism (which of course, is determined by the DNA of its genotype). This also includes (and/or determines) how that organism’s body responds to a given physical agent (a pharmaceutical, a toxin, sunlight, etc.). For example, genetically fair-skinned people tend to get sunburned easier/faster than other

people do. See also GENOTYPE, DEOXYRIBONUCLEIC ACID (DNA), MORPHOLOGY, GENE,

HAPLOTYPE, GENE EXPRESSION PROFILING.

Phenylalanine (phe) An essential amino acid. L-Phenylalanine is one of the raw materials u s e d t o m a n u f a c t u r e N u t r a S w e e t ® (NutraSweet Co.) synthetic sweetener. See

also LEVOROTARY (L) ISOMER, ESSENTIAL AMINO ACIDS, STEREOISOMERS.

Pheromones From the Greek words pherein, to carry, and hormon, to excite, they are sex hormones emitted by insects and animals; they spread through the air by the wind and diffusion for the purposes of attracting the opposite sex. Some pheromones have been produced artificially and used in lure traps to attract and catch male insects so as to prevent their mating with females (i.e., a biological pesticide). Pheromone traps for Japanese beetles are commonplace in infested areas (e.g., when utilizing Integrated Pest Management). It is envisioned that commercial exploitation of this area of science will increase. See also HORMONE,

INTEGRATED PEST MANAGEMENT (IPM).

Philadelphia Chromosome Refers to a particular human chromosome that is (visibly) distorted by the mutated gene that results in the disease known as chronic myelogenous leukemia (abbreviated CML, also known as chronic myeloid leukemia). That is because that gene codes for extensive production of the tyrosine kinase known as Bcr-Ab1; an enzyme which causes neoplastic (aberrant) cell growth and cell division. As a result, people with CML disease tend to have 10–25 times more white blood cells than normal. The pharmaceutical known as Gleevec™ induces apoptosis — “programmed” (selfdestruct) cell death — in the cells that have the Philadelphia chromosome; thus leading to cessation of CML. See also CHROMOSOMES,

KARYOTYPE, KARYOTYPER, GENE, CODING

SEQUENCE, MUTATION, CANCER, CELL, WHITE

BLOOD CELLS, GLEEVEC, APOPTOSIS.

Phosphate Transporter Genes Gene(s) within

 

the genomes of at least some plants, which

 

code for proteins that enable/increase the

 

ability of those plants to extract and utilize

 

phosphate (form of phosphorous) from the

 

soil. Since all plants require phosphorous for

 

proper growth and functioning, yet most

 

plants are not inherently very adept at

 

extracting and utilizing soil phosphate, add-

 

ing (more) phosphate transporter genes to a

 

given (crop) plant is likely to increase that

 

plant’s growth and yield (e.g., of seeds). See

 

also GENE, GENETIC ENGINEERING.

 

Phosphate-Group Energy The decrease in

 

free energy as one mole of a phosphorylated

 

compound at 1.0 M concentration undergoes

 

hydrolysis to equilibrium at pH 7.0 and 25°C

 

(77°F). The energy that is available to do

 

biochemical work. The energy arises from

 

the breakage (cleavage) of a phosphate to

 

phosphate bond. See also FREE ENERGY,

 

HYDROLYSIS, FATS, MOLE, PHOSPHOLIPIDS.

 

Phosphatidyl Choline See LECITHIN.

 

Phosphinothricin Another name for the her-

 

bicide active ingredient glufosinate. See also

 

GLUFOSINATE, PHOSPHINOTHRICIN ACETYLTRANS-

 

FERASE (PAT), PAT GENE, BAR GENE.

 

Phosphinothricin Acetyltransferase (PAT)

 

P

An enzyme which degrades (breaks down)

 

phosphinothricin (also known as glufosi-

 

 

nate), which is an active ingredient in some

 

herbicides. PAT is naturally produced in

 

some strains of soil bacteria (e.g., Strepto-

 

myces viridochromogenes). If a gene (called

 

the “PAT gene”) that codes for the produc-

 

tion of phosphinothricin acetyltransferase is

 

inserted via genetic engineering into a crop

 

plant’s genome, that would enable such

 

plants to survive post-emergence applica-

 

tions of phosphinothricin-containing herbi-

 

cides. See also ENZYME, PHOSPHINOTHRICIN,

 

GLUFOSINATE, BACTERIA, GENE, PAT GENE,

 

GENETIC ENGINEERING, GENOME, BAR GENE,

 

MARKER (GENETIC MARKER).

 

Phosphinotricine See PHOSPHINOTHRICIN.

 

Phosphodiesterases A category of enzymes

 

that inhibit apoptosis. Abbreviation for this

 

term (category) is PDE. See also ENZYME,

 

APOPTOSIS.

 

© 2002 by CRC Press LLC