Nature's pesticides

Ames, Bruce N.; Profet, Margie

doi:10.1002/nt.2620010103

Cited by 7 publications

(2 citation statements)

References 4 publications

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“…Exogenous additions to such endogenous contributors to the load ofoxidants are, e.g., oxides of nitrogen (NO) in cigarette smoke, generation of radicals from peroxides promoted by iron and copper compounds (Fenton reaction), and products from normal food intake (46,47). As a matter of fact, the effects of some anticancer drugs are based on this principle.…”

Section: Growth Of the Field Of Mitochondrial Diseasementioning

confidence: 99%

The development of mitochondrial medicine.

Luft¹

1994

Proc. Natl. Acad. Sci. U.S.A.

272

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Primary defects in mitochondrial function are implicated in over 100 diseses, and the list continues to grow. Yet the first mitochondrial defect-a myopathy-was demonstrated only 35 years ago. The field's dramatic expansion reflects growth of knowledge in three areas: (i) characterization of mitochondrial structure and function, (i) euiation of the steps involved in mitochondrial biosynthesis, and (Ni) discovery of specific mitochondrial DNA. Many mitochondrial diseases are accompanied by mutations in this DNA. Inheritance is by maternal t ission. The metabolic defects encompass the electron transport complexes, intermediates of the tricarboxylic acid cycle, and substrate transport. The clinical manifestations are protean, most often involving skeletal muscie and the central nervous system. In addition to being a primary cause of disease, mitochondrial DNA mutations and impaired oxidation have now been found to occur as secondary phenomena in aging as weli as in age-related degenerative diseases such as Parkinson, Alzheimer, and Huntington diseases, amyotrophic lateral sclerosis and cardiomyopathies, atherosclerosis, and diabetes meflitus. Manifestations of both the primary and secondary mitochondrial diseases are thought to result from the production of oxygen free radicals. With increased understanding of the mechanisms underlying the mitochondrial dysfunctions has come the beginnings of therapeutic sttegies, based mostly on the administration of antioxidants, replacement of cofactors, and provision of nutrients. At the present accelerating pace of development of what may be cafled mitochondrial medicine, much more is likely to be achieved within the next few years.In 1959, the first biochemical studies of a cell organelle in humans were undertaken, following observations made at the bedside of a patient with striking symptoms, never before encountered. These clinical observations, first, led to an idea about the origin ofthe symptoms and, second, to studies of the particular organelle: the mitochondrion (1). The pathophysiology of the mitochondria developed gradually over the years as relevant discoveries were made in biochemistry, cell biology, and molecular biology. During the past few years the field mitochondrial medicine has expanded dramatically, in several directions. I here provide a short review concentrating on those aspects most relevant to clinical medicine. In the accompanying review (174), Wallace describes the molecular, biological, and evolutionary implications of mitochondrial diseases.The Birth of Mitochondrial Medicine (1959)(1960)(1961)(1962): Luft DiseaseThe first patient found to have a mitochondrial disease was a 30-year-old woman who developed clinical symptoms at the age of 7. Her dominant symptoms were enormous perspiration combined with markedly increased fluid intake but without polyuria; extremely high caloric intake (above 3000 kcal per day) at a stable body weight of 38 kg and a body height of 159 cm; and general weakness, particularly prominent in her musculature. The do...

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Section: Growth Of the Field Of Mitochondrial Diseasementioning

confidence: 99%

The development of mitochondrial medicine.

Luft¹

1994

Proc. Natl. Acad. Sci. U.S.A.

272

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“…As a mechanism of defense, plants have developed a variety of toxic chemical compounds, with toxicity varying from relatively low (e.g., hydrogen cyanide acting as deterrent) to high (e.g., ptaquiloside [PTA], which causes carcinogenesis) [1,2]. These natural toxins are abundant in the environment and, hence, have the potential to pollute soils and water [3]. Pollution of groundwater and surface waters can be abated if the toxins are degraded or sorbed during transport through the soil matrix to aquifers or other recipients.…”

Section: Introductionmentioning

confidence: 99%

Degradation kinetics of ptaquiloside in soil and soil solution

Ovesen

Rasmussen²,

Hansen

2008

Environmental Toxicology and Chemistry

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Ptaquiloside (PTA) is a carcinogenic norsesquiterpene glycoside produced in bracken (Pteridium aquilinum (L.) Kuhn), a widespread, aggressive weed. Transfer of PTA to soil and soil solution eventually may contaminate groundwater and surface water. Degradation rates of PTA were quantified in soil and soil solutions in sandy and clayey soils subjected to high natural PTA loads from bracken stands. Degradation kinetics in moist soil could be fitted with the sum of a fast and a slow first-order reaction; the fast reaction contributed 20 to 50% of the total degradation of PTA. The fast reaction was similar in all horizons, with the rate constant k(1F) ranging between 0.23 and 1.5/h. The slow degradation, with the rate constant k(1S) ranging between 0.00067 and 0.029/ h, was more than twice as fast in topsoils compared to subsoils, which is attributable to higher microbial activity in topsoils. Experiments with sterile controls confirmed that nonmicrobial degradation processes constituted more than 90% of the fast degradation and 50% of the slow degradation. The lower nonmicrobial degradation rate observed in the clayey compared with the sandy soil is attributed to a stabilizing effect of PTA by clay silicates. Ptaquiloside appeared to be stable in all soil solutions, in which no degradation was observed within a period of 28 d, in strong contrast to previous studies of hydrolysis rates in artificial aqueous electrolytes. The present study predicts that the risk of PTA leaching is controlled mainly by the residence time of pore water in soil, soil microbial activity, and content of organic matter and clay silicates.

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