Radiation liver

As mentioned above, many transcription factors are not always active. Rather the activity of transcription factors is often achieved by induced reversible modification. Most frequently is the addition of phosphate groups (phosphorylation) to Ser, Thr, or Tyr residues. For the AP-1 component c-Jun the phosphorylation at Ser63 and Ser73 enhances activity when cells are subjected to stress, e.g. radiation. Phosphorylation is, however, dispensable for c-Jun-dqDendent tissue homeostasis in the liver, indicating that certain activities do not require the regulatory enhancement. Jun-N-teiminal kinase and a kinase called RSK or p38 catalyze the phosphorylation of AP-1. 

Lai, E.K., Crossley, C., Sridhar, R., Misra, H.P., Janzen, E.G. and McCay, P.B. (1986). / wro spin-trapping of free radicals generated in brain, spleen, and liver during gamma radiation of mice. Arch. Biochem. Biophys. 244, 156-160. 

Sinusoidal damage from cirrhosis is the most common cause of portal hypertension. The sinusoids are porous vessels within the liver that surround radiating rows of hepatocytes, the basic functional cells of the liver (Fig. 19-2). Progressive destruction of hepatocytes and an increase in fibroblasts and connective tissue surrounding the hepatocytes culminate in cirrhosis. Fibrosis and regenerative nodules of scar tissue... 

The model is designed to calculate the 241 Am intake that would produce the maximum allowed occupational radiation dose to all major organs, including the bone surfaces, bone marrow, and liver, but the conversion factors for other tissues and organs are published in the same tables. 

The Leggett (1992) model was developed to predict tissue doses and whole-body dose to people who may be exposed to americium. The model is considered an updated version of the ICRP (1989) model for americium, which has been used to establish risk-based limits of intake of241 Am (ICRP 1989). The Leggett (1992) and ICRP (1989) models predict similar long-term average doses of americium to the liver and skeleton for an injection exposure and would be expected to predict similar radiation risks and risk-based intake limits (Leggett 1992). Descriptions of applications of the Leggett (1992) model in risk assessment have not been reported. 

The model is designed to calculate americium excretion and time courses for americium levels in the liver, skeleton, and gonads. This output could be used to predict radiation doses to these tissues. 

Gruner R, Seidel A, Winter R. 1981. The initial early distribution of monomeric 239Pu and 241Am in rat liver as determined by triton WR 1339 injection. Radiat Res 85 367-379. 

Lloyd RD, Mays CW. 1975. Determining liver retention of transuranium elements in living beagles. Radiat Environ Biophys 12 139-145. 

Stover BJ, Bruenger FW, Stevens W. 1970. Association of americium with ferritin in the canine liver. Radiat Res 43 173-186. 

Siitterlin U, Thies W-G, Haffher H, et al. 1984. Comparative studies on the lysosomal association of monomeric 239Pu and 241Am in rat and Chinese hamster liver Analysis with sucrose, metrizamide, and percoll density gradients of subcellular binding as dependent on time. Radiat Res 98 293-306. 

Taylor GN, Lloyd RD, Mays CW, et al. 1992. Promotion of radiation-induced liver neoplasia by ethanol. Health Phys 62(2) 178-182. 

When not complexed, lanthanide ions have a high affinity for bone in vivo because they act as calcium ion mimics. Because the lanthanides undergo hydrolysis above a pH of 4, they readily form radiocolloids when not complexed, and are then taken up by the liver. This bone and liver uptake results in non-specific radiation doses to non-target (normal) tissues and organs and is undesirable.91 The polyaminocarboxylate class of ligands are considered to be the optimal choice for the basis of BFCAs for the+3 metal cations, including the lanthanides. It is essential that the... 

Radiation adversely affects limb regeneration of amphibians, alters DNA metabolism, and increases the frequency of chromosomal aberrations and liver lesions (Table 32.25). In some species of amphibians and reptiles, as in many mammals, mortality rates after acute exposure to radiation do not stabilize within 30 days — effectively invalidating the conventional LD50 (30-day postexposure) value. In the rough-skinned newt (Taricha granulosa), for example, the minimal LD50 dose at 200 days after irradiation was 2.5 Gy, compared with 350 Gy at 30 days (Willis and... 

Long-term health effects from exposure to low-to-moderate doses of radiation include cancer of the thyroid, prostate, kidney, liver, salivary glands, and lungs Hodgkin s disease leukemia and increased numbers of stillbirths and genetic defects. Concerns about potential long-term health effects often lead to anxiety and depression problems among those exposed to radiation. 

---