The impact of maternal high-fat diet on offspring neurodevelopment.

A maternal high-fat diet affects offspring neurodevelopment with long-term consequences on their brain health and behavior. During the past three decades, obesity has rapidly increased in the whole human population worldwide, including women of reproductive age. It is known that maternal obesity caused by a high-fat diet may lead to neurodevelopmental disorders in their offspring, such as autism spectrum disorder, attention deficit hyperactivity disorder, anxiety, depression, and schizophrenia. A maternal high-fat diet can affect offspring neurodevelopment due to inflammatory activation of the maternal gut, adipose tissue, and placenta, mirrored by increased levels of pro-inflammatory cytokines in both maternal and fetal circulation. Furthermore, a maternal high fat diet causes gut microbial dysbiosis further contributing to increased inflammatory milieu during pregnancy and lactation, thus disturbing both prenatal and postnatal neurodevelopment of the offspring. In addition, global molecular and cellular changes in the offspring's brain may occur due to epigenetic modifications including the downregulation of brain-derived neurotrophic factor (BDNF) expression and the activation of the endocannabinoid system. These neurodevelopmental aberrations are reflected in behavioral deficits observed in animals, corresponding to behavioral phenotypes of certain neurodevelopmental disorders in humans. Here we reviewed recent findings from rodent models and from human studies to reveal potential mechanisms by which a maternal high-fat diet interferes with the neurodevelopment of the offspring.

DNA-Damaging Effect of Different Wavelength (206 and 257 nm) Femtosecond Laser Pulses.

Objective: The purpose of this study was to investigate the possible cytotoxic and genotoxic impact of new-generation 206 nm femtosecond solid-state laser irradiation on murine skin cells in vitro, and to compare the cell and DNA damage caused by different wavelength (206 vs. 257 nm) femtosecond laser pulses. Background data: The first attempts to evaluate the possible genotoxic impact of ultrashort laser pulses on the murine bone marrow cells in vitro revealed the unlooked-for DNA-damaging effect. However, the impact of far-ultraviolet (UV) radiation on genetic material of internal and external organs' cells may differ due to differences in size, structure, and biochemical composition of the cells. Methods: Mouse skin cells were exposed to different doses of 206 and 257 nm wavelength femtosecond laser, and 254 nm UV lamp irradiation. Comet assay in two versions-the standard alkaline and the enzyme-linked-was used for the evaluation of DNA damage. Results: The irradiation determined by different parameters demonstrated intensity-dependent genotoxic impact. The pyrimidine dimers made up the greater part of DNA photodamage, but with rising exposure dose the increase of relative amount of more energy-consuming primary damage-DNA strand breaks-was detected. Conclusions: The 206 nm femtosecond laser irradiation was much more cytotoxic but caused less primary DNA damage than the same pulse duration longer wavelength (257 nm) laser irradiation. DNA-damaging effect of 206 nm femtosecond laser pulses with extremely low penetration force may highly depend on the size, structure, and biochemical composition of the cells of organ or tissue targets.