Ethylene Glycol Ethers Induce Oxidative Stress in the Rat Brain

Abstract

Ethylene glycol ethers (EGEs) are components of many industrial and household products. Their hemolytic and gonadotoxic effects are relatively well known while their potential adverse effects on the central nervous system have not yet been clearly demonstrated. The aim of the present study was to examine the effects of 4-week administration of 2-buthoxyethanol (BE), 2-phenoxyethanol (PHE) and 2-ethoxyethanol (EE) on the total antioxidant capacity, activity of some antioxidant enzymes, such as the superoxide dismutase (SOD), catalase, glutathione peroxidase (GPX) and glutathione reductase and lipid peroxidation in the frontal cortex and hippocampus in the rat. These studies showed that BE and PHE decreased the total antioxidant activity, SOD and GPX activity, while increased lipid peroxidation in the frontal cortex. Like in the frontal cortex, also in the hippocampus BE and PHE attenuated the total antioxidant activity, however, lipid peroxidation was increased only in animals which received BE while reduction in GPX activity was present in rats administered PHE. The obtained data indicated that 4-week administration of BE and PHE, but not EE, reduced the total antioxidant activity and enhanced lipid peroxidation in the brain. In the frontal cortex, adverse effects of PHE and BE on lipid peroxidation probably depended on reduction in SOD and GPX activity, however, in the hippocampus the changes in the total antioxidant activity and lipid peroxidation were not connected with reduction of the investigated antioxidant enzyme activity.

Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain

“…No difference was observed on brain TAC between sedentary (0.45±0.0 mM/µg protein) and trained animals (0.45±0.0 mM/µg protein) (P>0.05; Figure 3B ). Moreover, the basal data (sedentary values) are in agreement with others studies in the literature for SOD activity ( 12 ) and FRAP assay ( 13 ).…”

Prenatal Exposure to Glycol Ethers and Neurocognitive Abilities in 6-Year-Old Children: The PELAGIE Cohort Study

“…NMDA receptors are crucial to the synaptic plasticity and memory and learning processes related to the hippocampus (Shapiro 2001), and hippocampal volume was correlated with the WISC–IV Full-Scale IQ score ( r = 0.54, p < 0.05), and in particular with the WISC-VCI ( r = 0.69, p < 0.01), in 22 children 8–18 years old (Schumann et al 2007). Pomierny et al (2014) suggested that EGPhE can induce oxidative stress and enhance lipid peroxidation in the frontal cortex and hippocampus of rats, but these findings might not be a specific sign of neurotoxicity. In addition, rats were exposed subcutaneously at doses described as higher than the exposure levels experienced by humans, either in occupational settings or environmentally (Pomierny et al 2013).…”

The negative impact of the environment on methylation/epigenetic marking in gametes and embryos: A plea for action to protect the fertility of future generations

“…DEHPs have been classified as epigenetic carcinogens, and they also induce DNA strand breaks and chromosomal aberrations, as measured by several in vitro and in vivo tests (Ames test, unscheduled DNA synthesis, comet assay). Glycol ethers are also potential inducers of OS (Pomierny et al, ), and these are found in glass cleaning products, deodorants, perfumes, and even in medicine adjuncts. Metabolites of ethylene glycol, rather than ethylene glycol itself, are toxic and mutagenic (rat embryo; Klug, Merker, & Jäckh, ).…”