Immunohistochemical study of alpha-fetoprotein in the postnatal ontogeny of mice with a varying sensitivity to liver carcinogens]

The ontogenesis of alpha-fetoprotein (AFP) was studied in the C57BL, CC57BR, C3H/He, A/He and DD mice during the first 4 weeks of life. The AFP hepatocytes were determined by indirect immunofluorescent staining of liver cells isolated with sodium tetraphenyl borate; the content of AFP in blood was determined by the method of rado immunodiffusion. The methods utilized allowed to obtain the quantitative characteristics of the dynamics of AFP-positive cells in the liver and the content of AFP in the blood. In the newborn mice over 90% hepatocytes contain AFP, the intensity of luminescence being heterogenous. The number of bright-liminescent cells equals to 50% during the first day of life rapidly decreases and none of them are found by 9--11 days. The number of average- and weak-luminescent hepatocytes does not decrease during the first 10 days, but then gradually decreases and none of them are found by 23 days in the CC57BR and by 27 days in the DD and A/He mice. A comparison of the dynamics of AFP-positive cells in the liver and the content of AFP in the blood has shown that the bright-luminescent hepatocytes are the main producent of this protein in the early postnatal ontogenesis.     

Increased activity of phosphate-dependent glutaminase in liver mitochondria as a result of glucagon treatment of rats.

1. Injection of rats with glucagon leads to an increased effective activity of glutaminase in subsequently isolated liver mitochondria. 2. This effect of glucagon is manifested as a decreased requirement of glutaminase for phosphate in the presence of HCO3-. The HCO3--concentration-dependence is unchanged. 3. The effect of glucagon is lost on disruption of the mitochondria. 4. In accordance with previous reports, incubation of mitochondria in hypo-osmotic media also increases the effective activity of glutaminase. Glucagon increases glutamine hydrolysis at intermediate osmolarities of the suspending medium, but does not affect glutaminase activity when it is already maximally activated by hypo-osmotic conditions. 5. From this and previous work, it seems that hypo-osmotic incubation conditions, EDTA and glucagon may all activate glutaminase by a common mechanism. It is postulated that this mechanism involves modification of the interaction of glutaminase with the mitochondrial inner membrane.     

Alterations in liver mitochondrial function as a result of fasting and exhaustive exercise

Two-dimensional displays of the restriction fragments from the DNA of Mus musculus revealed a complex species-specific pattern produced from nonsatellite repetitive sequences. The patterns have been used as a guide in the direct purification of a group of broadly interspersed repeated DNA sequences (characterized by a 1350-bp Eco-Bam fragment) that have been studied by molecular cloning, restriction mapping and genomic Southern blotting. These studies show that the cloned representatives originate from an abundant group of sequences that share homology with about 2% of the mouse genome. The sequences do not appear to share homology with mouse-interspersed-family-1 (MIF-1) nor with the major AT-rich satellite sequences of mouse. They appear to be part of a group of larger repetitive elements that is both broadly interspersed and heavily methylated in normal mouse tissue.     

Antigenic variation and increase in pathogenicity in Pseudomonas aeruginosa as a result of growth on glucose or N-hexadecane as sole carbon source.

When Pseudomonas aeruginosa is grown on glucose as opposed to n-hexadecane as the sole carbon source, the antigenicity, virulence, and protein composition of the outer membrane are altered. The hydrocarbon-grown cells demonstrate a 3-log increase in virulence over the glucose-grown cells (in mice). There also appears to be an additional protein present in the outer membrane of the n-hexadecane-grown cells. This protein may contribute to the observed antigenic differences between the two cell types.     

Age-related differences in the effect of osmotic pressure on liver mitochondrial respiration in rats]

The subject under investigation is the influence of osmotic pressure of incubation medium (25-500 mM of sucrose) upon the respiration and the respiration control (RC) of mitochondria of the liver of rats aged 1, 3, 12 and 24 months when oxidizing succinate. In a medium with 0.3 M of sucrose the respiration rate under condition 3 (V3) and RC increased from the age of 1 to 12 months and decreased by 24 months. In a medium with 0.15 M of sucrose the age differences have not been observed. In a uncoupling state the osmotic dependence of the respiration of mitochondria of 1- and 12-month-old rats did not vary. It is assumed that with age there is a change in the rate of structural coupling of the carrier of adenine nucleotides with H(+)-ATP synthetase complex and (or) the viscosity of the matrix.     

Alpha-fetoprotein in the liver of embryonic and newborn rats]

The localization of alpha-fetoprotein in the liver of embryos and newborn Wistar rats was determined by the method of fluorescent antibodies. This protein was found in the cytoplasm of some hepatocytes, endothelium of blood vessels and erythroid blood cells of embryos and new born rats. It was never found in the blood-forming and Kupffer cells of the liver, as well as in the epithelium of bile ducts. The hepatocytes containing this protein were located in the liver lobes near the central veins. Their number and the intensity of fluorescence decreased with the age of animals.     

肝再生剌激因子对小鼠实验性急性肝损伤的保护作用

A hepatic stimulator substance (HSS) was extracted from the liver of male weanling SD rats according to the method of LaBrecque. The mice were injected with carbon tetrachloride or D-galactosamine to induce hepatic injuries and the protective effect of HSS on thus induced hepatic damage was investigated. The results were as follows: (1) HSS could suppresses the elevation of sGPT and sGOT induced by carbon tetrachloride intoxication in a dose-dependent manner. (2) Hepatic histological findings indicated that the degree of CCl4 or D-galactosamine-induced hepatic lesions could be lessened by HSS. (3) CCl4-induced reduction of hepatic mitochondrial succinic dehydrogenase activity could be restored by HSS. (4) Insulin-glucagon enhanced the survival of D-galactosamine intoxicated mice and stimulated hepatocyte proliferation, thus showing less pronounced hepatic damage.     

Dysfunctions of the epididymis as a result of primary carnitine deficiency in juvenile visceral steatosis mice

The juvenile visceral steatosis mutant mice serve as an animal model of primary carnitine deficiency, classified as the sudden infant death syndrome. The defect in carnitine uptake was recently found to be due to a defect in the carnitine transporter gene. We herein report, for the first time, the characteristics of epididymal dysfunction in juvenile visceral steatosis mice. At 8-9 weeks of age, the epididymis was deformed and weight was significantly increased. Histologically, the duct of the proximal epididymis was dilated due to the accumulation of an unusually high level of spermatozoa. Spermatozoa were extravasated from the epididymal duct into the stroma. In contrast, the duct of the distal epididymis was constricted and contained no spermatozoa. Thus, the epididymal disorder causes obstructive azoospermia, leading to infertility.     

An XXY mouse, the result of a rearrangement between one X and a Y chromosome

A male mouse with irregular white spotting, typical of piebald, s, arose during an experiment designed to search for mutations induced in spermatogonial cells by ethylnitrosourea (ENU). On being examined cytologically it was found to carry 40 chromosomes but was effectively XXY since one of the two X chromosomes present was distally fused to a Y chromosome. In common with the previously described XXY mice, all of which carried 41 chromosomes, the mouse was sterile with a total absence of germ cells. Because of this, it was not possible to determine if the white spotting was inherited. The spotting could not be related to any observable abnormality of chromosomes known to carry spotting genes, nor could it be linked in any way with the X and Y fusion. It was concluded from the cytological considerations and the time interval (6 months) that had elapsed between mutagen treatment and birth of the offspring, that whereas the spotting was probably the result of ENU damage in a spermatogonial stem cell, the XY fusion was probably a later and spontaneous event.     

Teratogenic effect of trifluoperazine in rats and mice

Trifluoperazine was administered to pregnant mice and rats by gastric intubation during the period of organogenesis. Dams were treated at doses of 0.5, 5, 50 (mice and rats) and 100 (only rats) mg/kg/day. The drug affected the pregnant weight increment in a dose-related manner in rats but only the 50 mg/kg/day dose level affected the weight gain of mice. The foetal weight was not markedly affected in either species. The drug induced cleft palate and micrognathia in rats but did not produce a teratogenic effect in mice. Trifluoperazine caused abortions in mice and there were significant increases in the number of resorptions with the top dose levels in both species.     

Skeletal morphology of inbred rats during hypokinesia and variants as a result of rehabilitation

Statistically significant dependence between physical loading and drug treatment in hypokinesia, on the one hand, and bone adaptation, on the other hand, was shown. Correction variants studied were expressed unequally in the animals of different strains. This indicates genetic growth determination and formation of limb bones.