The effect of zinc deficiency on deoxyribonucleic acid synthesis in rat liver

The effect of a short-term (3-day) dietary zinc deficiency on DNA synthesis in regenerating rat liver was investigated, with particular attention being paid to the timing of the S-phase of synthesis. The findings indicated a significantly reduced (P<0,01) incorporation of 'H-thymidine into the DNA of animals receiving the zinc-deficient ration (0,3 µg/g) when compared with control animals which received 60 µg/g in their diet. Of special interest was the finding that a shift occurred in the timing of the peak of maximum incorporation, from 17½ hours postoperatively in the control animals to 25 hours postoperatively in the deficient animals. Thus, when comparisons were made between the incorporation data at the respective peaks of maximum DNA synthesis, the effect of zinc deficiency was considerably reduced (P<0,05), but not eliminated when compared with the data obtained at the same time postoperatively in both groups. The data highlight the need for studies concerning the effect of zinc deficiency on the incorporation of 'Hthymidine to be performed at the peak of maximum DNA synthesis for the respective treatments, and not, as is done at present, at the same time for all groups.S. Afr. Med. J., 48, 1697 (1974)

Radioimmunological evaluation of rabbit anti-sera to ovine luteinizing hormone

No Abstrac

Zinc and inflammatory/immune response in aging

Life-long antigenic burden determines a condition of chronic inflammation, with increased lymphocyte activation and proinflammatory cytokine production. A large number of studies have documented changes in zinc metabolism in experimental animal models of acute and chronic inflammation and in human chronic inflammatory conditions. In particular, modification of zinc plasma concentration, as well as intracellular disturbance of antioxidant intracellular pathways, has been found in aging and in some age-related diseases. Zinc deficiency is diffused in aged individuals in order to avoid meat and other high zinc content foods due to fear of cholesterol. Rather, they increase the consumption of refined wheat products that lack zinc and other critical nutrients as a consequence of the refining process. On the other hand, plasma zinc concentration is influenced by proinflammatory cytokines (IL-6 and TNF-alpha) and by metallothioneins (MT) homeostasis, which is in turn affected by proinflammatory cytokines. MT increase in aging and chronic inflammation allowing a continuous sequestration of intracellular zinc with subsequent low zinc ion availability against stressor agents and inflammation. This phenomenon leads to an impaired inflammatory/immune response in the elderly. A major target of zinc is NF-kappa B, a transcription factor critical for the expression of proinflammatory cytokines whose production is regulated by extra- and intracellular activating and inhibiting factors interacting with the regulatory elements on cytokine genes. Effects of zinc on translocation of NF-kappa B have been attributed to the suppression of phosphorylation and degradation of the inhibitory proteins (A20) that normally sequester it in the cytoplasm. Moreover, this factor and A20 are regulated by specific genes involved in inflammation and by intracellular zinc ion availability. So, it is not so surprising that zinc deficiency is constantly observed in chronic inflammation, such as in old individuals. On the other hand, cytokine genes are highly polymorphic and some of these polymorphisms are associated with atherosclerosis and diabetes type 2. Therefore, zinc turnover, via MT homeostasis, in individuals genetically predisposed to a dysregulation of the inflammatory/immune response may play a crucial role in causing possible adverse events with the appearance of age-related diseases