Identity and virulence properties of Aeromonas isolates from healthy Northern snakehead (Channa argus) in China.

Members of the genus Aeromonas are opportunistic pathogen of a variety of aquatic animals that exhibits multidrug resistance, phenotypes, virulence genes and virulence. The present study described the species distribution and the potential pathogenicity of Aeromonas isolated from healthy Northern snakehead (Channa argus) in China. Molecular identification revealed that A. veronii biovar veronii (69/167; 41·3%) and A. hydrophila (41/167; 24·6%) were the most common species found in Northern snakehead intestine based on sequencing of the 16S rRNA gene and DNA gyrase subunit B protein. The distribution of seven virulence factors including aer (84·4%), act (80·8%), ser (40·1%), Aha (27·5%), lip (23·4%), exu (15·0%) and LuxS (12·6%) were determined exclusively in Aeromonas isolates. All the seven virulence genes were present in 9·6% (16/167), among which 11 strains were identified as A. veronii biovar veronii. For the strains harbouring seven virulence genes, the 50% lethal doses (LD50 ) of isolates were lower compared to the isolates carrying two virulence genes. The challenge tests revealed that isolate W31 had the lowest lethal dose, causing 50% mortality at 4·5 × 103 colony-forming units (CFU) per ml. Furthermore, histopathology of Northern snakehead infected with Aeromonas strains showed necrosis and congestion in liver, spleen and kidney and also damage to the intestine. This study confirms that the Aeromonas strains isolated from healthy Northern snakehead may be a cause of concern for public health. SIGNIFICANCE AND IMPACT OF THE STUDY: Aeromonas species are widely distributed in aquatic environments and have considerable virulence potential. The aim of this study was to identify Aeromonas strains isolated from healthy Northern snakehead, and to investigate if Aeromonas species isolated from healthy fish potential pathogenicity with special reference to virulence and epidemiology studies.

Systemic excretion of benzo(a)pyrene in the control and microsomally induced rat: the influence of plasma lipoproteins and albumin as carrier molecules.

In vitro studies have previously indicated that benzo(a)pyrene distributes primarily into the plasma lipoprotein fraction when incubated with whole plasma. Hydroxylated metabolites of benzo(a)pyrene distribute increasingly into the albumin fraction as the degree of metabolite hydroxylation increases. This report assesses the influence of plasma lipoproteins and albumin as carriers for benzo(a)pyrene on carcinogen excretion in the control and microsomally induced rat. Male Sprague-Dawley rats cannulated in the bile duct received i.v. injections of radiolabeled benzo(a)pyrene noncovalently bound to the very-low-density, low-density, or high-density lipoproteins in equimolar amounts. Bile was collected and measured for radioactivity. Cumulative biliary excretions of benzo(a)pyrene complexed with rat lipoproteins were 39.6 +/- 9.7 (S.D.), 24.6 +/- 1.3, and 21.2 +/- 8.8% for very low-density, low-density, and high-density lipoprotein, respectively. Values for excretion of benzo(a)pyrene complexed with rat or human lipoproteins were comparable. These data suggest that the transport molecule can effect a 2-fold difference in benzo(a)pyrene excretion under conditions of the present study. We infer that metabolism of the plasma lipoprotein molecules determines, in part, the extent of benzo(a)pyrene excretion. Cumulative biliary excretions of albumin-bound benzo(a)pyrene, 3-hydroxybenzo(a)pyrene, benzo(a)pyrene 7,8-dihydrodiol, and benzo(a)pyrene-4,5-epoxide were 28.0 +/- 2.7, 39.8 +/- 0.5, 46.9 +/- 2.5, and 49.8 +/- 1.2%, respectively. Thus, excretion increased as the degree of benzo(a)pyrene hydroxylation increased. The effect of microsomal enzyme induction on excretion of lipoprotein-bound benzo(a)pyrene was also assessed. Contrary to expectation, excretion of benzo(a)pyrene bound to the very-low-density, low-density, or high-density lipoproteins in Aroclor-induced rats was not greater than that of control animals. Hence, under the conditions of the present study, 60 to 80% of the injected benzo(a)pyrene and 50 to 60% of the injected benzo(a)pyrene metabolites were not excreted immediately in control or microsomally induced animals. This benzo(a)pyrene may represent a carcinogen pool that is slowly excreted.

Uptake of lipophilic carcinogens by plasma lipoproteins. Structure-activity studies.

This report describes the interaction between plasma lipoproteins and two hydroxylated metabolites of benzo[a]pyrene, 3-hydroxybenzo[a]pyrene and benzo[a]pyrene-7,8-dihydrodiol, which differ significantly in lipophilicity. When incubated with plasma, the metabolites of benzo[a]pyrene exhibit a decreasing distribution into the ultracentrifugal lipoprotein fraction (d less than or equal to 1.20) and an increasing distribution into the albumin-rich fraction (d greater than 1.20) as the degree of hydroxylation of the metabolite increases. At saturation, uptake of benzo[a]pyrene by VLDL, LDL and HDL correlates with lipoprotein and total-lipid volume. Uptake of hydroxylated derivatives per lipoprotein total-lipid volume, in general, decreases with increasing hydroxylation. Contrary to this trend, HDL uptake of 3-hydroxybenzo[a]pyrene at saturation is significantly higher than its uptake of benzo[a]pyrene. Uptake of benzo[a]pyrene-7,8-dihydrodiol per total-lipid volume by all of the lipoprotein classes at saturation is considerably lower than their uptake of 3-hydroxybenzo[a]pyrene. Factors in addition to lipid solubility substantially alter lipoprotein uptake of the metabolites.

[Effect of some factors on the development of exoerythrocytic stage of Plasmodium yoelii].

Using orthogonal design, the effect of environmental temperature, photoperiod, splenectomy and oestrogen levels upon the development of exoerythrocytic forms (EEF) of P. yoelii was observed. The results indicated that a significant number of viable sporozoites were cleared in the spleen, since the EEF density was much higher in the livers of splenectomized rats (1.73/mm3) than in sham-operated counterparts (0.55/mm3). The effect of high level oestrogen on EEF density was also evident since there was a significant difference between experimental (0.86) and control rats (1.42). Low environmental temperature caused the development of EEF stunted and asynchronous, but no significant effect on the density of EEF in this group was found. The density and average diameter (AD) of EEF between rats illuminated 8 and 16 hours per day were identical. The interaction between splenectomy and elevated oestrogen level offset each other, whereas the interactions between other two factors showed no difference by analysis of variance.

Nitroaromatic carcinogens in diesel soot: a review of laboratory findings.

The automobile industry plans to increase production of diesel-powered passenger cars because diesel engines provide better fuel economy than conventional gasoline engines. Diesel engines, however, produce more soot, and increased use of diesel cars will result in more discharge of diesel soot into the atmosphere. Recently, a new class of chemicals, called nitroaromatic compounds, have been identified in chemical extracts of diesel soot. Some of these nitroaromatic compounds produce mutations when tested in in vitro bacterial and mammalian cell assays, and cancer when tested in animals. Here, we review the relevance of these new laboratory findings to current deliberations over emission standards for particles from diesel cars.

A critical examination of assumptions used in risk assessments of dioxin contaminated soil.

Environmental standards for 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin, TCDD) are currently being considered by regulatory agencies worldwide. Among these are limits for tap water, soil at industrial sites, residential soil, fish, ambient air, and fly ash. Thus far, in the United States, no standards have been promulgated but a few have been suggested. This paper critically evaluates several aspects of previously proposed approaches to setting limits for TCDD in residential soil and soil within industrial sites. Factors and assumptions which significantly affect the predicted degree of hazard associated with exposure to soil contaminated with low levels of dioxin are discussed. This paper shows how different, more justifiable assumptions than those used by the Centers for Disease Control (CDC) regarding the quantities of soil typically consumed by children, TCDD's nongenotoxicity, dermal exposure to soil, the concentration of airborne soil particles, dioxin's bioavailability in soil, and extrapolation of the dose response curve can profoundly affect the results of the risk assessment and, subsequently, the magnitude of the recommended limits. Two case studies which quantitatively illustrate the effect of these assumptions on the risk estimates are presented. Non-U.S. regulatory agencies have considered TCDD's nongenotoxicity in estimating that the virtually safe dose (VSD) or acceptable daily dose for dioxin is approximately 10 pg/kg/day (10,000 fg/kg/day). These approaches are compared and contrasted with the method used by the United States EPA whose risk estimates are higher and whose VSD is approximately 1,000-fold lower. Alternative approaches to interpreting the cancer data indicate that a VSD of 130 pg/kg/day is more scientifically justified than risks estimated using standard approaches. This assessment indicates that a soil concentration of TCDD considerably in excess of 1 ppb should be acceptable for residential and nonresidential areas.

A critical evaluation of the use of mutagenesis, carcinogenesis, and tumor promotion data in a cancer risk assessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Regulatory agencies in the Western Hemisphere are currently assessing the potential human health risks of environmental contamination by 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). Some U.S. agencies such as the Environmental Protection Agency (EPA) and Centers for Disease Control (CDC) have assumed that TCDD behaves as a tumor initiator in animals and have used linear low-dose mathematical extrapolation models for estimating any human risk. In contrast, the Ontario Ministry of the Environment, the State Institute of National Health of The Netherlands, and the Federal Environmental Agency of the Federal Republic of Germany have concluded that TCDD does not have initiator activity; these agencies have advocated a risk extrapolation approach which applies a safety factor to a no-observable-effect level. Estimations of the potential risk obtained by these two approaches can differ by three to four orders of magnitude and have a major impact on the allocation of resources within the affected countries. This paper critically reviews the TCDD bacterial, animal, and human data on mutagenesis, carcinogenesis, and tumor promotion and concludes that the scientific evidence does not support risk estimations which are based on TCDD as a tumor initiator. Rather, the animal data overwhelmingly support TCDD as a tumor promoter. Risk estimations which incorporate tumor promotion activity more accurately reflect the scientific understanding of TCDD's mechanism of action and provide better estimates of its risk.