Environmental monitoring and the developmental origins of health and disease

Abstract

Early-life chronic exposure to environmental contaminants, such as bisphenol-A, particulate matter air pollution, organophosphorus pesticides, and pharmaceutical drugs, among others, may affect central tissues, such as the hypothalamus, and peripheral tissues, such as the endocrine pancreas, causing inflammation and apoptosis with severe implications to the metabolism. The Developmental Origins of Health and Disease (DOHaD) concept articulates events in developmental phases of life, such as intrauterine, lactation, and adolescence, to later-life metabolism and health. These developmental phases are more susceptible to environmental changes, such as those caused by environmental contaminants, which may predispose individuals to obesity, metabolic syndrome, and chronic noncommunicable diseases later in life. Alterations in the epigenome are explored as an underlying mechanism to the programming effects on metabolism, as the expression of key genes related with central and peripheral metabolic functions may be altered in response to environmental disturbances. Studies show that environmental contaminants may affect gene expressions in mammals, especially when exposed to during the developmental phases of life, leading to metabolic disorders in adulthood. In this review, we discuss the current obesity epidemics, the DOHaD concept, pollutants’ toxicology, environmental control, and the role of environmental contaminants in the central and peripheral programming of obesity and metabolic syndrome. Improving environmental monitoring may directly affect the quality of life of the population and help protect the future generations from metabolic diseases.

Influence of paternal consumption of a high-fat/high-sugar diet and/or orange juice during preconception on C57BL/6 female mice offspring breast cancer risk

“…This was later explained by the modifications of the epigenetic machinery, which influences gene expression and are inherited from one cell generation to the next, causing long lasting changes in gene expression and in organ structure (GOYAL; LIMESAND; GOYAL, 2019). Because key developmental stages such as preconception, lactation, early childhood and puberty are important in influencing long-term phenotypes (EL-HEIS et al, 2018;ALMEIDA et al, 2019), the term fetal programming has been substituted to Developmental Origins of Health and Disease (DOHaD) (NYIRENDA; BYASS, 2019).…”

“…There are limited studies in the literature on polyphenols in the context of paternal programming (SILVA et al, 2019). McPherson et al, (2016) evaluated in a rat model whether programming effects of paternal undernutrition could be prevented by supplementation with a mixture of green tea extract, lycopene and micronutrients (vitamin C, vitamin E, folate, zinc and selenium). The authors observed that paternal supplementation with the BFC/micronutrient mix was able to reduce oxidative damage to DNA and restored global methylation patterns in paternal sperm, preventing fat accumulation and dyslipidemia in offspring (MCPHERSON et al, 2016).…”

“…After washes, sections were incubated with the LABS + System -HRP Kit (Dako-Agilent Technologies, USA) and stained with 3,3'-diaminobenzidine in chromogen solution (Dako-Agilent Technologies, USA) for 2 min, washed and counterstained for 1.5 min with hematoxylin. Cell proliferation was quantified by assessing the number of Ki67 positive cells among 1,000 cells per structure (ducts or lobules) (GUIDO et al, 2016). H3K27me3 was evaluated by the intensity of the histone and quantified by the amount of specific stain present in a virtual slide by evaluating an average intensity of all pixels for subsequent calculation of optical density according to Pogribny et al, (2011).…”

“…H3K27me3 was evaluated by the intensity of the histone and quantified by the amount of specific stain present in a virtual slide by evaluating an average intensity of all pixels for subsequent calculation of optical density according to Pogribny et al, (2011). Apoptosis analysis was performed according to Elmore et al, (2016). The results are represented as mean number of apoptotic cells/1,000 cells per structure (ducts or lobules).…”

“…Alfaradhi et al (2016) observed that lean male offspring of obese dams presented increased adipose tissue TNF-a expression, which the authors attributed to miRNAs regulating expression of inflammatory signaling molecules. Consumption of orange juice by obese fathers reduced adipose tissue TNF-a expression and increased plasma GPx activity of female offspring when compared to OB offspring.…”