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Heavy metal contamination of agricultural fields has become a global concern as it causes a direct impact on human health. Rice is the major food crop for almost half of the world population and is grown under diverse environmental conditions, including heavy metal-contaminated soil. In recent years, the impact of heavy metal contamination on rice yield and grain quality has been shown through multiple approaches. In this review article, different aspects of heavy metal stress, that is uptake, transport, signaling and tolerance mechanisms, are comprehensively discussed with special emphasis on rice. For uptake, some of the transporters have specificity to one or two metal ions, whereas many other transporters are able to transport many different ions. After uptake, the intercellular signaling is mediated through different signaling pathways involving the regulation of various hormones, alteration of calcium levels, and the activation of mitogen-activated protein kinases. Heavy metal stress signals from various intermediate molecules activate various transcription factors, which triggers the expression of various antioxidant enzymes. Activated antioxidant enzymes then scavenge various reactive oxygen species, which eventually leads to stress tolerance in plants. Non-enzymatic antioxidants, such as ascorbate, metalloids, and even metal-binding peptides (metallothionein and phytochelatin) can also help to reduce metal toxicity in plants. Genetic engineering has been successfully used in rice and many other crops to increase metal tolerance and reduce heavy metals accumulation. A comprehensive understanding of uptake, transport, signaling, and tolerance mechanisms will help to grow rice plants in agricultural fields with less heavy metal accumulation in grains.

Dietary restriction (DR) has long been viewed as the most robust nongenetic means to extend lifespan and healthspan. Many aging-associated mechanisms are nutrient responsive, but despite the ubiquitous functions of these pathways, the benefits of DR often vary among individuals and even among tissues within an individual, challenging the aging research field. Furthermore, it is often assumed that lifespan interventions like DR will also extend healthspan, which is thus often ignored in aging studies. In this review, we provide an overview of DR as an intervention and discuss the mechanisms by which it affects lifespan and various healthspan measures. We also review studies that demonstrate exceptions to the standing paradigm of DR being beneficial, thus raising new questions that future studies must address. We detail critical factors for the proposed field of precision nutrigeroscience, which would utilize individualized treatments and predict outcomes using biomarkers based on genotype, sex, tissue, and age.

Evaluation of nutritionally enhanced biofortified dietary interventions that increase lifespan may uncover cost-effective and sustainable approaches for treatment of age-related morbidities and increasing healthy life expectancy. In this study, we report that anthocyanin rich, high yielding crossbred blue wheat prolongs lifespan of Drosophila melanogaster in different dietary contexts. In addition to functioning as an antioxidant rich intervention, the biofortified blue wheat also works through modulating expression of DR pathway genes including AMPK alpha, SREBP, PEPCK and Cry. Supplementation with blue- or purple-colored wheat provided better protection against paraquat-induced oxidative stress than control diet and increased survivability of flies in which superoxide dismutase 2 was knocked down conditionally in adults. Lastly, our findings indicate that supplementing biofortified blue wheat formulated diet prevented the decrease in lifespan and cardiac structural pathologies associated with intake of high fat diet. Overall, our findings indicate that plant-based diets formulated with biofortified cereal crops promote healthy ageing and delay progression of diseases that are exacerbated by accumulation of oxidative damage.

Dietary restriction (DR) extends healthy lifespan in diverse species. Age and nutrient-related changes in the abundance of microRNAs (miRNAs) and their processing factors have been linked to organismal longevity. However, the mechanisms by which they modulate lifespan and the tissue-specific role of miRNA mediated networks in DR dependent enhancement of lifespan remains largely unexplored. We show that two neuronally enriched and highly conserved microRNAs, miR-125 and let-7 mediate the DR response in Drosophila melanogaster. Functional characterization of miR-125 demonstrates its role in neurons while its target chinmo acts both in neurons and the fat body to modulate fat metabolism and longevity. Proteomic analysis revealed that Chinmo exerts its DR effects by regulating expression of FATP, CG2017, CG9577, CG17554, CG5009, CG8778, CG9527 and FASN1. Our findings identify miR-125 as a conserved effector of DR pathway and open up the avenue for this small RNA molecule and its downstream effectors to be considered as potential drug candidates for treatment of late-onset diseases and biomarkers for healthy aging in humans.