Total Liver DNA Research Articles

Cell division, cell death and hepatic DNA in relation to liver hypertrophy and regression in breeding ewes

SummaryLactation in ewes is associated with hypertrophy of the liver, due to cell proliferation and enlargement. The mean diameter of hepatic parenchymal cell nuclei increased after parturition to reach a maximum at 6 weeks, after which there was a decline.The liver regressed in weight after weaning but total DNA declined less than liver weight and remained elevated in comparison with livers of unmated ewes, while DNA concentration increased. Total liver DNA remained relatively high for approximately 6 months. It is suggested that the final fall to control values was associated with cell death and disorganization of the hepatic parenchyma.These results imply that the life span of one type of liver parenchymal cell may be at least 6 months.

Inhibition by chloramphenicol of aminoazo dye carcinogenesis in rat liver: studies of biochemical changes in rat liver and protein binding of carcinogen

A comparison of protein-bound dye levels in rat liver following the pair-feeding of diets containing either 3'-methyl-4-dimethylaminoazobenzene (3'MeDAB) 0.06% or 3'MeDAB 0.06% plus chloramphenicol 2% for periods of between 4 and 20 days has been made. No significant difference in this parameter was noted between the 2 groups. Further studies of changes in liver weight and composition following pairfeeding ( a) a control diet and diets containing ( b) chloramphenicol 2% ( c) 3'Me-DAB 0.06% and ( d) 3'MeDAB 0.06% plus chloramphenicol 2% for similar periods were also undertaken. There was progressive enlargement of the liver in all treated groups with the greatest increase taking place in rats which had received both 3'Me-DAB and chloramphenicol. Total liver protein and RNA were increased in rats receiving the chloramphenicol-containing diets and total liver DNA was increased in rats receiving the 3'MeDAB-containing diets. As a result of these changes, the liver RNA-DNA ratio was increased in rats receiving the chloramphenicol-containing diet, decreased in rats receiving the 3'MeDAB-containing diet and was normal in the control rats and the rats receiving both compounds. The findings suggest that the normal RNA-DNA ratio in the livers of rats fed both 3'MeDAB and chloramphenicol might be relevant to the protection against hepatocarcinogenesis afforded by this drug. The respective roles of macromolecular-bound derivatives of azo dyes and a mitotic response in the process of hepatocarcinogenesis in the rat are discussed in relation to the findings. It is suggested that the normal RNA-DNA ratio may be responsible for the normal mitotic response observed in the livers of the protected rats.

Incorporation of 32P i into mitochondrial and nuclear DNA in regenerating liver

32P i incorporation into the liver DNA of normal and hepatectomized rats was studied. Four h after injection of 32P 1 into normal rats the mitochondrial DNA had a specific activity 6 times as great as did nuclear DNA. Twelve h after hepatectomy a 4-h incorporation of 32P i showed that the specific activity of mitochondrial DNA was 18 times as great as that of nuclear DNA and accounted for 50% of the 32P i incorporated into the total liver DNA. At 24 h post hepatectomy the rate of nuclear synthesis of DNA reached a maximum and the specific activities of nuclear and mitochondrial DNA were then equal after a 4-h incorporation. When normal rats were injected with 32P i and sacrificed at times between 1 and 14 days after injection it was found that the specific activity of the mitochondrial DNA did not change appreciably during that period. In hepatectomized animals, both nuclear and mitochondrial DNA reached a maximum specific activity 2 days after injection and then both decayed at the same rate. The results indicate that mitochondrial DNA, like nuclear DNA, is metabolically stable and that DNA synthesis in normal ratliver mitochondria is a continuous process. The base ratios of mitochondrial and nuclear DNA were slightly but consistently different. A metabolically active contaminant associated with purified mitochondrial DNA after enzymatic digestion to mononucleotides was identified as AMP.

EFFECT OF A PROTEIN-FREE DIET ON PROTEIN METABOLISM IN THE PREGNANT RAT.

Estrone (0.5 Mg) and progesterone (6.0 μg) daily prevent the abortive effects of a protein-free diet but do not restore protein synthesis to normal levels in pregnant, protein-deficient rats. Thus, serum total protein, albumin, α1-globulin and A/G values were lower in protein-deficient, steroid-maintained rats than in rats pair-fed 20 % casein. Alanine and aspartic transaminase in uterus, placenta and liver were not altered by steroids or diet during pregnancy. Uteri, placentas and livers of protein-deficient, steroid-maintained rats weighed less and contained less total RNA and protein than did those of pair-fed controls, but total DNA in uterus and liver was not altered. Uterine and hepatic nucleic acids, as well as serum proteins and A/G ratios, were comparable in protein-deficient rats which maintained pregnancy with and without exogenous ovarian steroids. However, placenta] weight and total nucleic acids were greater in protein-deficient, injected rats than in uninjected rats fed the same diet. Possible mechanisms by which estrone and progesterone maintain pregnancy in protein-deficient rats are discussed, and it is suggested that steroids may maintain pregnancy, in the absence of dietary protein, by sustaining placental function. (Endocrinology76: 454, 1965)