Organic toxicants and plants.

Organic xenobiotics absorbed by roots and leaves of higher plants are translocated by different physiological mechanisms. The following pathways of xenobiotic detoxication have been observed in higher plants: conjugation with such endogenous compounds as peptides, sugars, amino acids, and organic acids; oxidative degradation and consequent oxidation of xenobiotics with the final participation of their carbon atoms in regular cell metabolism. The small parts of xenobiotics are excreted maintaining their original structure and configuration. Enzymes catalyze oxidative degradation of xenobiotics from the initial hydroxylation to their deep oxidation. The wide intracellular distribution and inductive nature of oxidative enzymes lead to the high detoxication ability. With plant aging, transformation of the monooxygenase system into peroxidase takes place. Once in the cells, xenobiotics are incorporated into different cell organelles. All xenobiotics examined are characterized by a negative effect on cell ultrastructure. The penetration of high doses of xenobiotics into plant cells leads to significant deviations from the norm and, in some cases, even to the complete cell destruction and plant death.

The cyanide leaching gold recovery process is a nonsustainable technology with unacceptable impacts on ecosystems and humans: the disaster in Romania.

The statements and discussions in this commentary are based on the disastrous situation near Baia Mare in Romania, where a dam of a cyanide basin burst on January 30, 2000, with serious consequences.

EDITORIAL

Copyright

Rudolf Wittenzellner (1921-1997)

Copyright 1997 Academic Press

Chronic inhalation exposure of rats to nitromethane.

Male and female Long-Evans rats were housed in inhalation chambers and exposed to vapors of nitromethane (NM) at either 100 or 200 ppm. The animals were exposed 7 hr per day, 5 days per week for 2 years. Control groups of rats were also housed in a similar inhalation chamber, but NM was not introduced into the chamber. The animals were observed daily for signs of pharmacologic or toxicologic effect and body weights were recorded periodically. At the 2-year termination of the exposure period, clinical laboratory examinations (serum chemistry and hematology) were performed on selected animals and all surviving animals were sacrificed. All animals were necropsied and subjected to a thorough histopathologic examination. During the study there were no pharmacologic effects from exposure to NM at either 100 or 200 ppm. There was no effect on mortality on either sex at either exposure level. Body weights of male rats exposed to NM were not significantly different from those of control rats, but the body weights of female rats of both exposure groups were slightly less than their controls. There was no effect of exposure of rats of either sex to either level of NM on hematology. There were no clinically significant effects on serum chemistry. There were no effects of exposure to NM on organ weights. There were no significant differences in the nonneoplastic or neoplastic pathology related to exposure to NM.

Safety assessment based on irrelevant toxicologic data: an extraordinary case of bromomethane used as a fumigant.

Bromomethane (BM) is a fumigant used in agriculture; it readily breaks down to bromide ion. WHO assessed the ADI of BM, at 1 mg/kg, using data on the toxicity of bromide. On the other hand, U.S. EPA used the observation of hyperplasia in the forestomach of rats given BM by gavage and arrived at a value of 0.0014 mg/kg. The validity of EPA's assessment is thus subject to question because of the data involved by (1) direct introduction of this volatile and reactive chemical to the GI by gavage and (2) using lesions in the rat forestomach which is absent in humans.

From single-substance evaluation to ecological process concept: the dilemma of processing gold with cyanide.

In the past decades, limit concentration values for environmentally dangerous synthetic and natural chemical substances have been established in industrialized countries. Depending on the range of application, state of aggregation, propagation velocity, specific action on living organisms, long- or short-time effect, etc., different terms are used to specify these limit concentrations (acceptable daily intakes, TLV, LD50, emission values, water quality standards, etc.). Several parameters (e.g., range of application, ethic and social valuation, environmental factors, scientific knowledge) have led to nationally and internationally varying values depending on the region and time. The accuracy of this system of evaluation cannot necessarily be improved by listing further analytical data, but rather by furnishing sufficiently secured scientific data for a serious discussion, with the public concepts influenced more and more by the mass media. The best-established scientific knowledge has been acquired by the chemical industry. National and international groups demand that ecological-chemical problems in other fields of industry be dealt with as well; this research should, without doubt, be intensified. The example of the mining industry, which must employ chemical methods to isolate small concentrations (ppm), demonstrates the environmental conflict caused by the increasing world population, requiring the adaptation of the process by industry to the modern environmental concept. This is illustrated by the evolution of the gold recovery process.

Effects of short-term inhalation exposure to 1-nitropropane and 2-nitropropane on rat liver enzymes.

Male Sprague-Dawley rats were exposed to vapors of 1-nitropropane (1-NP) and 2-nitropropane (2-NP) at air concentrations of 100 ppm for 7 hours per day on four consecutive days. Livers were analyzed for enzymatic activities after 1-, 2-, and 4-day inhalation periods. Liver microsomal cytochrome P450 was depressed by 2-NP and elevated following exposure to 1-NP. Levels of cytochrome b5 were slightly increased in rats exposed to 1-NP and remained unchanged after inhalation of 2-NP. Total glutathione (GSH), GSH S-transferase, and UDP-glucuronosyltransferase activities were enhanced by 2-NP. 1-NP induced GSH peroxidase while 2-NP did not. Glutathione reductase was not altered after exposure to either isomer. No changes in the microsomal malondialdehyde content as a measure of lipid peroxidation and in the levels of serum aspartate transferase and serum glutamic oxaloacetic transaminase were observed during a 4-day exposure period in either of the exposed groups compared to control animals.