Copper (Cu) is an essential micronutrient for both pathogens and the hosts during viral infection. Cu is involved in the functions of critical immune cells such as T helper cells, B cells, neutrophils natural killer (NK) cells, and macrophages. These blood cells are involved in the killing of infectious microbes, in cell-mediated immunity and the production of specific antibodies against the pathogens. Cu-deficient humans show an exceptional susceptibility to infections due to the decreased number and function of these blood cells. Besides, Cu can kill several infectious viruses such as bronchitis virus, poliovirus, human immunodeficiency virus type 1(HIV-1), other enveloped or nonenveloped, single- or double-stranded DNA and RNA viruses. Moreover, Cu has the potent capacity of contact killing of several viruses, including SARS‐CoV‐2. Since the current outbreak of the COVID-19 continues to develop, and there is no vaccine or drugs are currently available, the critical option is now to make the immune system competent to fight against the SARS‐CoV‐2. Based on available data, we hypothesize that enrichment of plasma copper levels will boost both the innate and adaptive immunity in people. Moreover, owing to its potent antiviral activities, Cu may also act as a preventive and therapeutic regime against COVID-19.

Despite the fact that the estrogenic effects of bisphenols were first described 80 years ago, recent data about its potential negative impact on birth outcome parameters raises a strong rationale to investigate further. The adverse health effects of plastics recommend to measure the impacts of endocrine‐disrupting compounds (EDCs) such as bisphenols (BPA, BPS, BPF), bis(2‐ethylhexyl) phthalate, and dibutyl phthalate (DBP) in human health. Exposure to these compounds in utero may program the diseases of the testis, prostate, kidney and abnormalities in the immune system, and cause tumors, uterine hemorrhage during pregnancy and polycystic ovary. These compounds also control the processes of epigenetic transgenerational inheritance of adult‐onset diseases by modulating DNA methylation and epimutations in reproductive cells. The early developmental stage is the most susceptible window for developmental and genomic programming. The critical stages of the events for a normal human birth lie between the many transitions occurring between spermatogenesis, egg fertilization and the fully formed fetus. As the cells begin to grow and differentiate, there are critical balances of hormones, and protein synthesis. Data are emerging on how these plastic‐derived compounds affect embryogenesis, placentation and feto‐placental development since pregnant women and unborn fetuses are often exposed to these factors during preconception and throughout gestation. Impaired early development that ultimately influences fetal outcomes is at the center of many developmental disorders and contributes an independent risk factor for adult chronic diseases. This review will summarize the current status on the impact of exposure to plastic derived EDCs on the growth, gene expression, epigenetic and angiogenic activities of the early fetal development process and their possible effects on birth outcomes.

Dietary components are essential for the structural and functional development of the brain. Among these, docosahexaenoic acid, 22:6n-3 (DHA), is critically necessary for the structure and development of the growing fetal brain in utero. DHA is the major n-3 long-chain polyunsaturated fatty acid in brain gray matter representing about 15% of all fatty acids in the human frontal cortex. DHA affects neurogenesis, neurotransmitter, synaptic plasticity and transmission, and signal transduction in the brain. Data from human and animal studies suggest that adequate levels of DHA in neural membranes are required for maturation of cortical astrocyte, neurovascular coupling, and glucose uptake and metabolism. Besides, some metabolites of DHA protect from oxidative tissue injury and stress in the brain. A low DHA level in the brain results in behavioral changes and is associated with learning difficulties and dementia. In humans, the third trimester-placental supply of maternal DHA to the growing fetus is critically important as the growing brain obligatory requires DHA during this window period. Besides, DHA is also involved in the early placentation process, essential for placental development. This underscores the importance of maternal intake of DHA for the structural and functional development of the brain. This review describes DHA’s multiple roles during gestation, lactation, and the consequences of its lower intake during pregnancy and postnatally on the 2019 brain development and function.

During pregnancy, maternal plasma fatty acids are critically required for cell growth and development, cell signaling, and the development of critical structural and functional aspects of the feto-placental unit. In addition, the fatty acids modulate the early stages of placental development by regulating angiogenesis in the first-trimester human placenta. Preferential transport of maternal plasma long-chain polyunsaturated fatty acids during the third trimester is critical for optimal fetal brain development. Maternal status such as obesity, diabetes, and dietary intakes may affect the functional changes in lipid metabolic processes in maternal-fetal lipid transport and metabolism. Fatty acids traverse the placental membranes via several plasma membrane fatty acid transport/binding proteins (FAT, FATP, p-FABPpm, and FFARs) and cytoplasmic fatty acid-binding proteins (FABPs). This review discusses the maternal metabolism of fatty acids and their effects on early placentation, placental fatty acid transport and metabolism, and their roles in feto-placental growth and development. The review also highlights how maternal fat metabolism modulates lipid processing, including transportation, esterification, and oxidation of fatty acids.

Fatty acids are essential for feto-placental growth and development. Maternal fatty acids and their metabolites are involved in every stage of pregnancy by supporting cell growth and development, cell signaling, and modulating other critical aspects of structural and functional processes. Early placentation process is critical for placental growth and function. Several fatty acids modulate angiogenesis as observed by increased tube formation and secretion of angiogenic growth factors in first-trimester human placental trophoblasts. Long-chain fatty acids stimulate angiogenesis in these cells via vascular endothelium growth factor (VEGF), angiopoietin-like protein 4 (ANGPTL4), fatty acid-binding proteins (FABPs), or eicosanoids. Inadequate placental angiogenesis and trophoblast invasion of the maternal decidua and uterine spiral arterioles leads to structural and functional deficiency of placenta, which contributes to preeclampsia, pre-term intrauterine growth restriction, and spontaneous abortion and also affects overall fetal growth and development. During the third trimester of pregnancy, placental preferential transport of maternal plasma long-chain polyunsaturated fatty acids is of critical importance for fetal growth and development. Fatty acids cross the placental microvillous and basal membranes by mainly via plasma membrane fatty acid transport system (FAT, FATP, p-FABPpm, & FFARs) and cytoplasmic FABPs. Besides, a member of the major facilitator superfamily-MFSD2a, present in the placenta is involved in the supply of DHA to the fetus. Maternal factors such as diet, obesity, endocrine, inflammation can modulate the expression and activity of the placental fatty acid transport activity and thereby impact feto-placental growth and development. In this review, we discuss the maternal dietary fatty acids, and placental transport and metabolism, and their roles in placental growth and development.

Cytokine-mediated inflammation is increasingly recognized for playing a vital role in the pathophysiology of a wide range of brain disorders, including neurodegenerative, psychiatric, and neurodevelopmental problems. Pro-inflammatory cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) cause neuroinflammation, alter brain function, and accelerate disease development. Despite progress in understanding these pathways, effective medicines targeting brain inflammation are still limited. Traditional anti-inflammatory and immunomodulatory drugs are effective in peripheral inflammatory illnesses. Still, they face substantial hurdles when applied to the central nervous system (CNS), such as the blood–brain barrier (BBB) and unwanted systemic effects. This review highlights the developing treatment techniques for modifying cytokine-driven neuroinflammation, focusing on advances that selectively target critical cytokines involved in brain pathology. Novel approaches, including cytokine-specific inhibitors, antibody-based therapeutics, gene- and RNA-based interventions, and sophisticated drug delivery systems like nanoparticles, show promise with respect to lowering neuroinflammation with greater specificity and safety. Furthermore, developments in biomarker discoveries and neuroimaging techniques are improving our ability to monitor inflammatory responses, allowing for more accurate and personalized treatment regimens. Preclinical and clinical trial data demonstrate the therapeutic potential of these tailored techniques. However, significant challenges remain, such as improving delivery across the BBB and reducing off-target effects. As research advances, the creation of personalized, cytokine-centered therapeutics has the potential to alter the therapy landscape for brain illnesses, giving patients hope for better results and a higher quality of life.