Determination of 3-chloro-1,2-propanediol in foods and food ingredients by gas chromatography with mass spectrometric detection: collaborative study.

The results of a collaborative study are reported for the determination of 3-chloro-1,2-propanediol (3-monochloropropane-1,2-diol; 3-MCPD) in a wide range of foods and food ingredients, using gas chromatography with mass spectrometric detection and incorporating the use of a deuterated internal standard. After a pretrial study, 12 laboratories (6 United Kingdom, 1 Switzerland, 1 Japan, 2 United States, 1 The Netherlands, and 1 from the European Commission) were asked to analyze 12 test materials (as known duplicates or split-level samples) by using a prescribed procedure. The test materials consisted of duplicate samples of acid-hydrolyzed vegetable protein (containing 3-MCPD at 0.029 mg/kg), malt extract (0.055 mg/kg), wholemeal bread crumbs (0.030 mg/kg), salami (0.016 mg/kg), cheese alternative (0.043 mg/kg), and soup powder (split levels at 0.045 and 0.041 mg/kg). Repeatability ranged from 0.005 to 0.013 mg/kg and reproducibility, from 0.010 to 0.027 mg/kg, for the samples tested. Precision values were well within statistically predicted levels (HORRAT values of <1 for 5 of the 6 matrixes tested) and within method criteria prepared by a joint working group composed of the United Kingdom Ministry of Agriculture, Fisheries and Food and industry representatives. The study demonstrated the satisfactory validation of the method for quantifying 3-MCPD at levels of > or = 0.010 mg/kg. The limit of detection derived from separate in-house studies was estimated to be 0.005 mg/kg. The method was adopted First Action by AOAC INTERNATIONAL.

Naturally occurring Brucella suis biovar 4 infection in a moose (Alces alces).

A debilitated adult female moose (Alces alces) shot east of the MacKenzie River, Northwest Territories, Canada, had large fluctuant masses over both carpi. Only the forelimbs were available for examination. Carpal pathology included bilateral bursitis and osteomyelitis of subjacent bone. In addition severe osteomyelitis with fractures was observed in the left lateral and right medial digits. Brucella suis biovar 4 was isolated from the right medial first phalanx. This is believed to be the first reported case of infection with this organism in a wild moose. The bacterium is common in caribou (Rangifer tarandus) in the region.

Vitamin A status of wild mallards (Anas platyrhynchos) wintering in Saskatchewan.

Vitamin A status of wild male mallards (Anas platyrhynchos) overwintering in Saskatchewan, Canada was determined. Vitamin A levels < 0.2 micrograms hepatic retinyl palmitate/g liver, occurred in 6% and 25% of male mallards sampled in 1991 to 1992 and 1992 to 1993, respectively. There was no temporal trend in vitamin A levels over either winter. Squamous metaplastic lesions, commonly associated with vitamin A deficiency in domestic animals, were not observed in any bird; hence, they were not a good indicator of vitamin A status in wild mallards. Serum retinol was not a good indicator of vitamin A status in wild mallards. Many mallards in good body condition had low vitamin A levels; thus, we propose that good body condition and ample fat stores are not indicative of overall health of the bird.

Experimental vitamin A deficiency in mallards (Anas platyrhynchos): lesions and tissue vitamin A levels.

Captive mallards (Anas platyrhynchos), fed an all-grain diet for up to 5 months during the winters of 1991 to 1992 and 1992 to 1993, developed lesions of squamous metaplasia; some had no detectable hepatic vitamin A. Vitamin A deficiency in mallards was defined as hepatic levels of retinyl palmitate < 2 micrograms/g liver. Lesions were found only in ducks with low levels of hepatic vitamin A, but not all ducks with these low levels of hepatic vitamin A had histological lesions. The prevalence of lesions in the esophagus was greatest cranially and caudally and less common in the central region. Palatine salivary glands rarely were affected. Mallards with liver stores > 600 micrograms of hepatic retinyl palmitate per g liver, fed a diet deficient in vitamin A were unlikely to become deficient over a 5 month period. Birds fed an all-grain diet had significantly lower vitamin A concentrations in their liver compared to those fed an all-grain diet with vitamin A added. Liver weight, when corrected for body size, did not affect vitamin A concentration. Serum retinol levels were conserved over a large range of hepatic vitamin A levels but levels below 300 micrograms retinol/l were useful in detecting vitamin A deficiency in captive mallards. Based on the findings, the presence of lesions provides a conservative measure of vitamin A status in ducks and tissue levels should be measured in instances when mallards have questionable vitamin A status.

Effects of vehicle exhaust emissions on urban wild plant species.

Very few investigations have examined the direct impacts of vehicle exhausts on plants and attempted to separate out the key pollutants responsible for observed effects. This paper describes a multi-phase investigation into this topic, using 12 herbaceous species typical of urban areas and representing different functional groups. Fumigations were conducted in solardomes with diesel exhaust pollutants at concentrations designed to simulate those close to a major highway in inner London. A wide range of effects were detected, including growth stimulation and inhibition, changes in gas exchange and premature leaf senescence. This was complemented by controlled fumigations with NO, NO(2) and their mixture, as well as a transect study away from a busy inner London road. All evidence suggested that NO(x) was the key phytotoxic component of exhaust emissions, and highlights the potential for detrimental effects of vehicle emissions on urban ecosystems.

T-2 toxin inhibits mitochondrial function in yeast.

T-2 toxin inhibits oxygen consumption of whole cells and purified mitochondria of Saccharomyces cerevisiae. Inhibition of mitochondrial respiration is not relieved by 2, 4-dinitrophenol, indicating that T-2 toxin inhibits mitochondrial function at the level of the electron transport chain. T-2 toxin inhibition of state 3 respiration (with succinate) is overcome by N, N, N', N'-tetramethyl-p-phenylenediamine, indicating inhibition of site II of the electron transport chain. T-2 toxin inhibits mitochondrial succinate dehydrogenase activity and increases mitochondrial NADH dehydrogenase activity.