Erratum: Altered gene expression linked to germline dysfunction following exposure to DEET.

[This corrects the article DOI: 10.1016/j.isci.2023.108699.].

Altered gene expression linked to germline dysfunction following exposure of Caenorhabditis elegans to DEET.

N,N-diethyl-meta-toluamide (DEET) is a commonly used synthetic insect repellent. Although the neurological effects of DEET have been widely investigated, its effects on the germline are less understood. Here, we show that exposure of the nematode Caenorhabditis elegans, which is highly predictive of mammalian reprotoxicity, resulting in internal DEET levels within the range detected in human biological samples, causes activation of p53/CEP-1-dependent germ cell apoptosis, altered meiotic recombination, chromosome abnormalities, and missegregation. RNA-sequencing analysis links DEET-induced alterations in the expression of genes related to redox processes and chromatin structure to reduced mitochondrial function, impaired DNA double-strand break repair progression, and defects during early embryogenesis. We propose that Caenorhabditis elegans exposure to DEET interferes with gene expression, leading to increased oxidative stress and altered chromatin structure, resulting in germline effects that pose a risk to reproductive health.

Exposure to phthalates: germline dysfunction and aneuploidy.

Epidemiological studies continue to reveal the enduring impact of exposures to environmental chemicals on human physiology, including our reproductive health. Phthalates, a well characterized class of endocrine disrupting chemicals and commonly utilized plasticizers, are among one of the many toxicants ubiquitously present in our environment. Phthalate exposure has been linked to increases in the rate of human aneuploidy, a phenomenon that is detected in 0.3% of livebirths resulting in genetic disorders including trisomy 21, approximately 4% of stillbirths, and over 35% of miscarriages. Here we review recent epidemiological and experimental studies that have examined the role that phthalates play in germline dysfunction, including increases in apoptosis, oxidative stress, DNA damage, and impaired genomic integrity, resulting in aneuploidy. We will further discuss subject variability, as it relates to diet and polymorphisms, and the sexual dimorphic effects of phthalate exposure, as it relates to sex-specific targets. Lastly, we discuss some of the conserved effects of phthalate exposure across humans, mammalian models and nonmammalian model organisms, highlighting the importance of using model organisms to our advantage for chemical risk assessment and unveiling potential mechanisms that underlie phthalate-induced reproductive health issues across species.