Zinc is a critical component in a number of conserved processes that regulate female germ cell growth, fertility, and pregnancy. During follicle development a sufficient intracellular concentration of zinc in the oocyte maintains meiotic arrest at prophase I until the germ cell is ready to undergo maturation. An adequate supply of zinc is necessary for the oocyte to form a fertilization-competent egg as dietary zinc deficiency (ZD) or chelation of zinc disrupts maturation and reduces oocyte quality. Following sperm fusion to the egg to initiate the acrosomal reaction, a quick release of zinc, known as the zinc spark, induces egg activation in addition to facilitating zona pellucida hardening and reducing sperm motility to prevent polyspermy. Symmetric division, proliferation, and differentiation of the pre-implantation embryo rely on zinc availability both during oocyte development and post-fertilization. Further, the fetal contribution to the placenta, fetal limb growth, and neural tube development are hindered in females challenged with ZD during pregnancy. In this review, we discuss the role of zinc in germ cell development, fertilization, and pregnancy with a focus on recent studies in mammalian females. We further detail the fundamental zinc-mediated reproductive processes that have only been explored in non-mammalian species and speculate on the role of zinc in similar mechanisms of female mammals. The evidence collected over the last decade highlights the necessity of zinc for normal fertility and healthy pregnancy outcomes which suggests zinc supplementation should be considered for reproductive age women at risk of ZD.

We tested the hypothesis that hesperidin would reverse age-related aortic stiffness, perivascular adipose (PVAT) mediated-arterial stiffening and PVAT advanced glycation end-products (AGE) accumulation. Aortic pulse wave velocity (aPWV) and intrinsic mechanical stiffness, two measures of arterial stiffness, were assessed in C57BL/6 mice that were young (6months), old (27-29months), or old treated with hesperidin for 4weeks. Old compared with young mice had increased aPWV (444±10 vs. 358±8cm/s, P<0.05) and mechanical stiffness (6506±369 vs. 3664±414kPa, P<0.05). In old mice hesperidin reduced both aPWV (331±38cm/s) and mechanical stiffness (4445±667kPa) to levels not different from young. Aortic segments from old animals cultured with (+) PVAT had greater mechanical stiffness compared to young (+) PVAT (6454±323 vs. 3575±440kPa, P<0.05) that was ameliorated in arteries from old hesperidin treated cultured (+) PVAT (2639±258kPa). Hesperidin also reversed the aging-related PVAT AGE accumulation (all, P<0.05). A 4-week treatment with the AGE inhibitor aminoguanidine reversed both the age-related increase in aPWV (390±7cm/s) and mechanical stiffness (3396±1072kPa), as well as mechanical stiffness in arteries cultured (+) PVAT (3292±716kPa) (all, P<0.05) to values not different from young. In conclusion, hesperidin ameliorates the age-related increase in aortic stiffness and the PVAT-mediated effects on arterial stiffening. Hesperidin also reversed PVAT AGE accumulation, where PVAT AGE were shown to promote aortic stiffness with aging.

Birth control and family planning play pivotal roles in the economic growth and reduction of maternal, infant, and child mortality. Current contraceptives, such as hormonal agents and intrauterine devices, target only a small subset of reproductive processes and can have serious side effects on the health of women. To develop novel contraceptive agents, a scalable microfluidic device is established for analyzing and screening the effects of potential contraceptive agents on the maturation of the cumulus–oocyte complex. The microfluidic device performs on‐chip incubation for studying oocyte maturation and cumulus expansion and isolates the microwells by oil–water interfaces to avoid crosstalk between the wells. A filter membrane is incorporated in the device to simplify incubation, medium exchange, washing, and fluorescence staining of oocytes. Cumulus expansion can be monitored directly in the device and oocyte maturation can be examined after enzymatic removal of cumulus cells and on‐chip fluorescence staining. The performance of the device is evaluated by studying the influence of three drugs known to block oocyte maturation and/or cumulus expansion.

We hypothesized a sweet potato intervention would prevent high-fat (HF) diet-induced aortic stiffness, which would be associated with decreased arterial oxidative stress and increased mitochondrial uncoupling. Young (8-week old) C57BL/6J mice were randomly divided into 4 groups: low fat (LF; 10% fat), HF (60% fat), low-fat sweet potato (LFSP; 10% fat containing 260.3 μg/kcal sweet potato), or high-fat sweet potato diet (HFSP; 60% fat containing 260.3 μg/kcal sweet potato) for 16 weeks. Compared with LF and LFSP, HF- and HFSP-fed mice had increased body mass and percent fat mass with lower percent lean mass (all, P < 0.05). Sweet potato intervention did not influence body composition (all, P > 0.05). Arterial stiffness, assessed by aortic pulse wave velocity and ex vivo mechanical testing of the elastin region elastic modulus (EEM) was greater in HF compared with LF and HFSP animals (all, P < 0.05). Advanced glycation end products and nitrotyrosine abundance were greater in aortic segments from HF mice compared with LF and HFSP animals (all, P < 0.05). Aortic elastin and uncoupling protein 2 expressions, however, were reduced in HF compared with LF and HFSP mice (all, P < 0.05). Aortic segments cultured with 2,4-dinitrophenol (DNP), a mitochondrial uncoupler, for 72 h reduced the EEM of HF arteries compared with nontreated HF segments (P < 0.05). DNP had no effect on the EEM of aortic segments from HFSP mice. In conclusion, sweet potato attenuates diet-induced aortic stiffness independent of body mass and composition, which is associated with a normalization of arterial oxidative stress possibly due to mitochondrial uncoupling.

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