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Biomedical subjects

R S Yang

Publications and source records attributed to R S Yang.

At least 145 records · Page 8Linked to original sources
PubMed1975

Chromatographic methods for the analysis of hexachlorobenzene and possible metabolites in monkey fecal samples.

The separation and identification of hexachlorobenzene (HCB), pentachlorobenzene (QCB), and pentachlorophenol (PCP) by thin layer, high-pressure liquid, and gas chromatography are reported. Satisfactory results were obtained with reverse phase thin layer and high-pressure liquid chromatography. The 2 gas chromatographic columns tested gave adequate separation of HCB and QCB. A PCP methylation process using dimethyl sulfate was attempted. Procedures are presented for extraction, cleanup, separation, and identification of HCB and possible metabolites from feces of a rhesus monkey treated with 14C-HCB. Recovery of radioactivity in excess of 96% was attained in extracts from feces by these methods. Preliminary evidence suggests the formation of PCP and possibly other polar metabolites from HCB in the rhesus monkey.

Animals↗
PubMed1973

Age-dependent arylsulphatase and sulphotransferase activities in the southern armyworm: a possible insect endocrine regulatory mechanism?

Arylsulphate and sulphotransferase activities were determined during the late larval development of the southern armyworm. Arylsulphatase titre attains a maximum during the moult and is at a minimum between moults. Sulphotransferase titre appeared to follow the inverse course. A possible enzymic regulatory mechanism for insect steroid hormones is discussed.

Animals↗
PubMed1972

Enzymic sulphation of p-nitrophenol and steroids by larval gut tissues of the southern armyworm (Prodenia evidania Cramer).

1. An enzyme system that catalyses the sulphation of p-nitrophenol, cholesterol, alpha-ecdysone, beta-sitosterol, dehydroepiandrosterone, oestrone and four other steroids of plant and insect origin was obtained from the soluble fraction of southern-armyworm gut tissues. 2. The enzyme system required ATP and inorganic sulphate, and activity was slightly enhanced in the presence of GSH. 3. The properties of this enzyme system with respect to pH, temperature, substrate and protein concentrations and various cofactors and reagents were studied. At -23 degrees C the enzyme preparation could be stored for 2 weeks without drastic loss of activity. At the end of storage for 1 month the loss of activity was approx. 21%. 4. The possible involvement of this enzyme system in insect endocrine control is discussed.

Adenosine Triphosphate↗
PubMedDate not supplied

Acute and subchronic toxicity of ethylenediamine in laboratory animals.

As part of a comprehensive toxicology program on ethylenediamine (EDA), acute, short-term repeated and subchronic toxicity studies were conducted. Ethylenediamine dihydrochloride (EDA X 2HCl) was used in these studies. EDA X 2HCl was slightly to moderately toxic to laboratory rats, mice or rabbits in the following acute tests: Peroral intubation, percutaneous administration, primary skin irritation and eye injury. Following dietary inclusion of EDA X 2HCl for 7 days at up to 2.70 g/kg/day to Fischer 344 rats or B6C3F1 mice, body weight gain and some organ weights of the animals were depressed in both sexes at the highest dose level. When Fischer 344 rats were fed EDA X 2HCl at 0, 0.05, 0.25, 1.00 g/kg/day for 3 months, marked decreases in body weight gain were observed in both sexes at the highest dose level. Other dose-related effects observed in either or both sexes primarily at the highest dose level, and for some at the intermediate dose level, included organ weight changes and alterations in some clinical chemistry, hematology and urinalysis parameters. No deaths occurred during the exposure period, nor were there any significant gross lesions in any of the animals. Histologic findings indicate a dose-related increase in hepatocellular pleomorphism and mild hepatocellular degeneration.

Animals↗
PubMedDate not supplied

Some current approaches for studying combination toxicology in chemical mixtures.

Using conventional toxicology methodologies and at the mode and rate of studying chemicals in the last 25 yr, it is doubtful that society will ever have adequate toxicology information on the majority of the chemicals we used now on in the future. Considering further the issue of health effects of chemical mixture exposure (i.e. real-world issues), the problem of not being able to obtain adequate toxicology information is amplified. From a different perspective, concerns over animal rights have raised the consciousness of many biomedical researchers regarding animal experimentation. As many as 17-100 million animals are estimated to be killed for biomedical research in the US alone each year; therefore, minimizing animal usage judiciously in toxicological research should be in the mind of every responsible toxicologist. From these considerations, it is apparent that new, alternative, less animal-intensive, shorter-term and less expensive toxicology methods must be developed if there is to be a reasonable chance to deal with the hundreds of thousand of chemicals, as well as the near-infinite number of chemical mixtures, in the environment. Some of the recent advances indeed are heading towards that direction. In this article, a number of approaches for research work on combination toxicology of chemical mixtures are given; the examples are selected based on one or more of the following criteria: (1) minimizing animal usage; (2) shortening experimental durations; (3) studying environmentally realistic concentrations; (4) utilizing statistical/mathematical modelling; (5) advancing efficient experimental designs and (6) developing predictive toxicology.

Animal Rights↗
PubMedDate not supplied

Toxicity testing of chemical mixtures: some general aspects and need of international guidelines.

The topics discussed by the Working Group on Toxicity Testing of Chemical Mixtures included the following (1) the study designs and results from two real-life exposure scenarios as additional information to the various investigations reported at the conference; (2) the need to take into consideration low-level, long-term exposure (i.e. mimicking human exposure conditions) as well as the issue of limited resources in experimental toxicology studies; (3) the importance of exploring alternative and predictive toxicology methodologies to minimize animal use and to conserve resources; (4) the realization that interactive toxicity should include the consideration of physical and biological agents in addition to chemicals. Two specific studies reported at the conference were also discussed. A number of recommendations were made concerning the planning and implementation of toxicology studies on chemical mixtures.

Animals↗
PubMedDate not supplied

1995 STP Young Investigator Award recipient. Increased rate of apoptosis correlates with hepatocellular proliferation in Fischer-344 rats following long-term exposure to a mixture of groundwater contaminants.

Apoptosis was evaluated in the livers of Fischer-344 rats following observations of increased hepatocellular proliferation from exposures, at low parts per million (ppm) levels, to a drinking water mixture of 7 groundwater contaminants during a 6-mo time-course study. The 7 chemicals used are among the most frequently detected contaminants associated with hazardous waste sites: arsenic, benzene, chloroform, chromium, lead, phenol, and trichloroethylene. Significant increases in 5-bromo-2'-deoxyuridine hepatocellular labeling were present in a unique pattern surrounding large hepatic veins (0.5-2.0 mm). This did not appear to be a regenerative response due to cytotoxicity, as assessed by the absence of increased plasma enzyme activity and the absence of hepatocellular lesions. Immunohistochemical staining for apoptosis, using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method showed patterns of labeling in treated animals that directly correlated to areas of increased hepatocyte proliferation. Apoptotic activity was maximum at the 1-mo exposure time point, whereas proliferating hepatocytes reached a maximum rate at the 10-day time point. This may have been triggered as a compensatory response to the increased cell proliferation or as a protective response to remove cells with altered DNA due to chemical mixture exposure. The principal findings of this paper are that (a) apoptosis directly correlated with changes in cell proliferation: (b) observed effects were produced by repeated exposures to a relatively low-level chemical mixture; and (c) the TUNEL method detected apoptotic cells at very early and late stages, potentially increasing the observable time period for apoptosis.

Animals↗