Performance of turkey poults fed different doses of aflatoxins in the diet.

This work was conduced to determine the performance parameters of initial-phase turkey poults fed 7 different doses of aflatoxins in the diet. Three hundred thirty-six 1-d-old male turkey poults were used in this research. Turkeys were divided into 7 treatments according to aflatoxin doses (T1 = control; T2 = 20 ppb aflatoxins; T3 = 50 ppb; T4 = 100 ppb; T5 = 200 ppb; T6 = 500 ppb; T7 = 1,000 ppb). Birds were killed in 2 periods: half of them after 21 d of experiment and the remaining birds after 42 d of experiment. In both periods, the evaluated parameters were as follows: feed consumption, BW, relative weights of organs (liver, gizzard, heart, and bursa of Fabricius) and meat (breast and thighs), and clinical biochemistry parameters (total plasmatic proteins, albumin, uric acid, cholesterol, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase). At 21 d of experiment, both feed consumption and BW were significantly affected by the aflatoxins present in the diet. Nevertheless, gizzard relative weight, total plasmatic proteins, and cholesterol levels were also affected. At the 42-d evaluation, besides feed consumption and BW, gizzard and liver relative weights and cholesterol levels were also affected by the presence of aflatoxins in the diet. Turkey poults are very sensitive to aflatoxin poisoning, because they are at least 3 to 6 times more sensitive to these contaminants than broilers.

Early ultrastructural changes during thioacetamide-induced apoptosis in rat liver.

An histological and ultrastructural study of the early changes in the liver following a single administration of thioacetamide (TH), was carried out in male Wistar rats. One hour after treatment, apoptosis was already present in the liver. By electron microscopy, the following sequential changes were observed: progressive detachment of hepatocytes from neighboring cells, formation of surface infolds with multiple blebs and, finally, release of several membrane-bounded apoptotic bodies in the extracellular space and into the sinusoidal lumen. Three hours after TH administration, the apoptotic cycle was almost entirely completed, as shown by the presence of phagocytosed apoptotic bodies inside the cytoplasm of intact liver cells. Our study evidences that TH induces apoptosis of liver cell as early as one hour after its administration. Moreover, our data show that the apoptotic cycle may be completed in 3-4 h. From the morphological point of view, apoptosis induced by TH appears indistinguishable from programmed cell death, occurring during embryogenesis or metamorphosis, and from apoptotic cell death seen during regression of mitogen-induced rat liver hyperplasia.

The surface composition and temperature of asteroid 21 Lutetia as observed by Rosetta/VIRTIS.

The Visible, InfraRed, and Thermal Imaging Spectrometer (VIRTIS) on Rosetta obtained hyperspectral images, spectral reflectance maps, and temperature maps of the asteroid 21 Lutetia. No absorption features, of either silicates or hydrated minerals, have been detected across the observed area in the spectral range from 0.4 to 3.5 micrometers. The surface temperature reaches a maximum value of 245 kelvin and correlates well with topographic features. The thermal inertia is in the range from 20 to 30 joules meter(-2) kelvin(-1) second(-0.5), comparable to a lunarlike powdery regolith. Spectral signatures of surface alteration, resulting from space weathering, seem to be missing. Lutetia is likely a remnant of the primordial planetesimal population, unaltered by differentiation processes and composed of chondritic materials of enstatitic or carbonaceous origin, dominated by iron-poor minerals that have not suffered aqueous alteration.

Induction of two different modes of cell death, apoptosis and necrosis, in rat liver after a single dose of thioacetamide.

A sequential study of the appearance of liver cell death after thioacetamide (TH) administration was performed in male Wistar rats. Within 3 hours of a single dose of TH, occurrence of cell death by apoptosis was evident around the centrilobular area. Light as well as electron microscopic examination demonstrated the presence of eosinophilic globules, often containing nuclear remnants (apoptotic bodies); they frequently were found within the cytoplasm of intact hepatocytes. The number of apoptotic bodies (ABs) was further enhanced at 6 hours, resulting in a 70-fold increase over the control values. Although necrosis or inflammation could not be observed at this time, as monitored by microscopic analysis as well as by determination of serum glutamate pyruvate transaminase levels, centrilobular necrosis accompanied by massive inflammatory reaction was evident at 12 hours and even more pronounced at 24 to 36 hours. Evidence of liver regeneration was found to occur at 48 hours, and the liver regained its normal architecture between 72 and 96 hours. Studies performed to analyze the activity of 'tissue' transglutaminase (tTG), a presumptive marker of apoptosis, showed that, 1 hour after treatment, TH caused a drastic dose-dependent inhibition of the enzyme activity. This early inhibition was followed by a rapid recovery in tTG activity that paralleled the induction of apoptosis in the liver. Treatment with cycloheximide (CH) 2 hours after TH partially inhibited the incidence of ABs at 6 hours (approximately 30% inhibition). The present study indicates that two different modes of cell death, apoptosis and necrosis, may be induced in a sequential fashion by a single dose of TH.

Mitogen-induced liver hyperplasia does not substitute for compensatory regeneration during promotion of chemical hepatocarcinogenesis.

Experiments were designed to determine the efficacy of different types of liver cell proliferative stimuli given during exposure to several liver tumor-promoting regimens, on the formation of foci of enzyme-altered hepatocytes. Male Wistar rats were initiated with diethylnitrosamine (150 mg/kg body wt). After a 2 week recovery period animals were subjected to promoting regimens, the resistant hepatocyte model, the phenobarbital model and the orotic acid model. While the rats were on these regimens they were given liver cell proliferative stimulus, either a compensatory type (two-thirds partial hepatectomy or a necrogenic dose of carbon tetrachloride) or a direct hyperplastic stimulus such as that induced by the primary mitogen, lead nitrate. Initiated cells so promoted by these regimens were monitored as foci of enzyme-altered hepatocytes positive for gamma-glutamyltransferase and placental glutathione S-transferase or deficient for adenosine triphosphatase. While carbon tetrachloride and partial hepatectomy-induced compensatory regeneration stimulated the promoting ability of the regimens used, direct hyperplasia could not stimulate the formation of foci and/or nodules from initiated hepatocytes. Evaluation of thymidine incorporation indicated that there was no significant difference in the extent of DNA synthesis in both the proliferative stimuli irrespective of the promoting procedure used.

Different effects of regenerative and direct mitogenic stimuli on the growth of initiated cells in the resistant hepatocyte model.

The possible mechanism(s) responsible for the different effects exerted by proliferative stimuli of different nature on the appearance of enzyme-altered hepatic foci, were investigated in male Wistar rats. Rats given an initiating dose of diethylnitrosamine (150 mg/kg body weight) were fed a diet containing 0.03% acetylaminofluorene for 2 weeks. Between the first and the second week, cell proliferation was induced by a proliferative stimulus of compensatory type (partial hepatectomy) or by a direct mitogenic stimulus (lead nitrate, 100 mumol/kg). The effect of the two different proliferative stimuli on the appearance of gamma-glutamyl transferase-positive foci was monitored by killing the rats for examination at 1, 2, 3, 5, and 6 days after the induction of cell proliferation. The results indicate that while enzyme-altered hepatocytes can be observed as early as 3 days after partial hepatectomy and are characterized by a rapid growth, direct hyperplasia did not exert any effect on the growth capacity of initiated cells. No effect of lead nitrate-induced hyperplasia was observed following three administrations of the mitogen. When platelet-poor plasma taken from animals exposed to the different proliferative stimuli was tested in primary cultures of hepatocytes, it was found that it induced a significant increase in the labeling index of normal hepatocytes. However, while serum taken 6 days after partial hepatectomy was still able to induce a significant increase in the labeling index, platelet-poor plasma from lead-treated rats had lost part of its effect at 5 days after treatment. The inability of direct hyperplasia to stimulate the development of enzyme-altered hepatic foci was not unique to lead nitrate since the same phenomenon was observed when three other hepatomitogens, nafenopin, cyproterone acetate, and ethylene dibromide, were used.