Effect of Maternal Marginal Zinc Deficiency on Development, Redox Status, and Gene Expression Related to Oxidation and Apoptosis in an Avian Embryo Model

Abstract

Maternal severe zinc (Zn) deficiency resulted in growth retardation and high mortality during embryonic development in human. Therefore, this study is aimed at evaluating the effect of maternal marginal Zn deficiency on the development and redox status to avoid severe Zn deficiency using an avian model. A total of 324 laying duck breeders at 214 days old were randomly allotted into 3 dietary Zn levels with 6 replicates of 18 ducks per replicate. The birds were fed experimental diets including 3 dietary supplemental Zn levels of 0 mg/kg (maternal Zn-deficient group, 29.2 mg Zn/kg diet), 60 mg/kg (maternal Zn-adequate group), and 120 mg/kg (maternal Zn-high group) for 6 weeks. Dietary Zn levels had on effect on egg production and fertility ( P > 0.05 ), whereas dietary Zn deficiency decreased breeder plasma Zn concentration and erythrocytic alkaline phosphatase activity at week 6 and inhibited erythrocytic 5 ′ -nucleotidase (5 ′ -NT) activity at weeks 2, 4, and 6 ( P < 0.05 ), indicating that marginal Zn-deficient status occurred after Zn depletion. Maternal marginal Zn deficiency increased embryonic mortality and contents of superoxide anion radical, MDA, and PPC and reduced MT content and CuZnSOD activity in duck embryonic livers on E29. The MDA content was positively correlated with embryonic mortality. Maternal marginal Zn deficiency increased BCL2-associated X protein and Caspase-9 mRNA expressions as well as decreased B-cell lymphoma-2 and MT1 mRNA and signal AKT1 and ERK1 protein expressions ( P < 0.05 ). Breeder plasma Zn concentration and erythrocytic 5 ′ -NT activities at week 6 were positively correlated with GSH-Px activity and GPx, MT1, and BCL2 mRNA expressions in embryonic livers on E29. In conclusion, erythrocytic 5 ′ -NT activity could be more rapid and reliable to monitor marginal Zn-deficient status. Marginal Zn deficiency impaired hatchability and antioxidant defense system and then induced oxidative damage and apoptosis in the embryonic liver, contributing to the greater loss of duck embryonic death.

Effects of Zinc Status on Expression of Zinc Transporters, Redox-Related Enzymes and Insulin-like Growth Factor in Asian Sea Bass Cells

“…Restricting our analysis to mRNA expression is a clear limitation of this study. Since the data shown for zinc transporters and MT presented here ( Figure 1 , Figure 2 and Figure 3 ) match well with major findings regarding zinc metabolism in other species [ 9 , 19 , 31 , 39 ], the validity of our data is still probably high. Unfortunately, the available resources for studying zinc transporters and zinc-related processes in Asian sea bass on a molecular level are so far limited.…”

“…In contrast, CAT activity was increased in the heart of zinc deficient rats and a slight increase in the activity of SOD was observed as well [ 47 ]. Embryos from zinc deficient ducks revealed higher expression and activities of CAT [ 39 ]. Moreover, thermal or nutritional stress significantly increased SOD mRNA and CAT levels in the tropical fish species Chanos chanos [ 48 ] and in plasma of Starry flounder [ 49 ].…”

Effect of Bis(maltolato)oxovanadium(IV) on Zinc, Copper, and Manganese Homeostasis and DMT1 mRNA Expression in Streptozotocin-Induced Hyperglycemic Rats

“…Studies conducted on fish reported that supplementation with Cu nanoparticles increased GPx, SOD and CAT activities and decreased MDA levels [ 50 ]. Gao et al found a positive correlation between plasma Zn content and GPx activity and a negative correlation between plasma Zn content and MDA content [ 51 ]. However, other authors negatively related serum Zn to GPx and positively to SOD and found no significant relationship with CAT and MDA content, whereas serum Cu content positively relates to GPx and negatively relates to SOD and CAT; no significant relationship with MDA was found [ 52 ].…”

Maternal zinc alleviates tert-butyl hydroperoxide-induced mitochondrial oxidative stress on embryonic development involving the activation of Nrf2/PGC-1α pathway

“…Many studies revealed that Zn as a cofactor of some distinct metalloenzymes is proposed to play a strong antioxidant role to restore mitochondrial oxidative damage [ 8 ]. Maternal Zn deficiency induces oxidative damage in liver resulting in embryonic development stagnation in the chick [ 9 ], duck [ 10 ] and mice [ 11 ]. Some studies have explored that maternal Zn supplementation could enhance the synthesis of hepatic metallothionein (MT) in offspring embryos [ 12 ], which is relevant in scavenging the excessive mitochondrial ROS generation under stressful conditions [ 13 ].…”