Zinc: A promising agent in dietary chemoprevention of cancer.

Proper intake of dietary nutrients is considered crucial for preventing the initiation of events leading to the development of carcinoma. Many dietary compounds have been considered to contribute in cancer prevention including zinc, which plays a pivotal role in host defense against the initiation and promotion of several malignancies. Zinc is an essential element that is integral to many proteins and transcription factors which regulate key cellular functions such as the response to oxidative stress, DNA replication, DNA damage repair, cell cycle progression, and apoptosis. Zinc has been ascribed roles in the metabolism and interaction of malignant cells, particularly in apoptosis. Zinc is involved in structural stabilization and activation of the p53 that appears to be an important component of the apoptotic process and also in activation of certain members of the caspase family of proteases. Zinc exerts a positive beneficial effect against chemically induced preneoplastic progression in rats and provides an effective dietary chemopreventive approach to disease in vulnerable section of population with family history of carcinoma. The present review provides an insight into the research conducted on animals as well as on human subjects for providing the concept that zinc deficiency is an important factor in the development and progression of malignancy and that zinc could be efficacious in the prevention and treatment of several cancers viz., colon, pancreas, oesophageal and head and neck. However, it needs further exploration with regard to other definitive bioassays including protein expression and documentation of specific molecular markers to establish the exact mechanism for zinc-mediated cancer chemoprevention. Preclinical trials need to investigate the genetic and epigenetic pathways of chemoprevention by zinc.

Zinc deficiency decreased cell viability both in endothelial EA.hy926 cells and mouse aortic culture ex vivo and its implication for anti-atherosclerosis

Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with TNFalpha for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy (15 micrometer Zn) or Zn-deficiency (0 micrometer Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various TNFalpha (0-30 mg/ml) and intracellular zinc chelator, N, N, N', N', -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, 0-30 microM) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-alpha treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-alpha and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.

Effect of Zinc on Peripheral Blood T-lymphocyte in the Duckling / 中国兽医学报

150-day-old Tianfu ducklings were divided into three groups,and fed with diets as follows :Zn deficient (22. 9 mgZn per kg diet),controls(100 mg Zn per kg diet) and Zn toxic (1 300 mg Zn per kg diet) for seven weeks (Zn deficiency,ZD)or four weeks (Zn toxieity,ZT). The ANAE+ positive ratios of the peripheral blood T-lymphocytes were much lower (P＜0.01 ) in Zn deficient and toxic groups than in the control group. The results showed that Zn deficiency and toxicity would suppress the development of T-lymphocytes and reduce the peripheral blood T-lymphocyte populations. Potential mechanisms underlying these observations are also discussed.

Effect of dietary zinc deficiency on the enzymatic components of free radical defense system in the skin of rats / 대한피부과학회지

The effect of dietary zinc deficiency on the enzymatic components of free radical defense system was observed in the skin of rats. We measured the concentration of serum zinc and the enzymatic activities of CuZn superoxide dismutase(CuZn SOD), glucose-6-phosphate dehydrogenase(GGPDH) and glutathione reductase (GSH-RD). The serum zinc level was sig nificantly lower in the zinc-deficient group compared to the zinc-supplemented group after 8 weeks of consuming the diet(P<0.01). CuZn SOD activity was not different between the two groups after 4 weeks. The Zn deficient group showed the significantly decreased activity of G6PDH after 4 and 8 weeks of consuming the diet(P<0.01). The activity of GSH-RD was increased in the zinc-deficient group compared to the supplemented group after 4 weeks of consuming the diet(P<0.01), but after 8 weeks the activity was not different between the two groups. From the results obtained, it could be concluded that GSH-RD may contribute to the oxygen free radical defense system in zinc deficiency in the earlier weeks of consum ing the zinc-deficient diet.

INFLUENCE OF ESSENTIAL FATTY ACID ON EXPERIMENTAL ZINC DEFICIENCY IN RATS / 营养学报

Low zinc (1.4-1.5 ppm) ration containing saturated fat (coconut oil) was fed to weanling rats, death occurred since second week. In third week, total death was 55%. The survivors manifested severe Zn-deficiency symptoms. When they were given Zn supplement in drinking water (100 ppm Zn), the deficient symptoms disappeared quickly and body weights increased rapidly. When coconut oil was replaced by safflower oil, the rats didn't show any Zn-deficiency symptom in 4 weeks. There was no difference in Zn contents of plasma and hair between Zn-deficient rats and the normals. Adjusting fatty acids composition of dietary fat to contain linoleic acid at 20% of total fatty acids, the rats manifested Zn-deficient symptoms after 2 weeks, and Zn contents of plasma and hair were significantly lower than that of normal rats(P