Environmentally toxicant exposures induced intragenerational transmission of liver abnormalities in mice

Abstract

Environmental toxicants such as chemicals, heavy metals, and pesticides have been shown to promote transgenerational inheritance of abnormal phenotypes and/or diseases to multiple subsequent generations following parental and/ or ancestral exposures. This study was designed to examine the potential transgenerational action of the environmental toxicant trichloroethane (TCE) on transmission of liver abnormality, and to elucidate the molecular etiology of hepatocyte cell damage. A total of thirty two healthy immature female albino mice were randomly divided into three equal groups as follows: a sham group, which did not receive any treatment; a vehicle group, which received corn oil alone, and TCE treated group (3 weeks, 100 μg/kg i.p., every 4 th day). The F0 and F1 generation control and TCE populations were sacrificed at the age of four months, and various abnormalities histpathologically investigated. Cell death and oxidative stress indices were also measured. The present study provides experimental evidence for the inheritance of environmentally induced liver abnormalities in mice. The results of this study show that exposure to the TCE promoted adult onset liver abnormalities in F0 female mice as well as unexposed F1 generation offspring. It is the first study to report a transgenerational liver abnormalities in the F1 generation mice through maternal line prior to gestation. This finding was based on careful evaluation of liver histopathological abnormalities, apoptosis of hepatocytes, and measurements of oxidative stress biomarkers (lipid peroxidation, protein carbonylation, and nitric oxide) in control and TCE populations. There was an increase in liver histopathological abnormalities, cell death, and oxidative lipid damage in F0 and F1 hepatic tissues of TCE treated group. In conclusion, this study showed that the biological and health impacts of environmental toxicant TCE do not end in maternal adults, but are passed on to offspring generations. Hence, linking observed liver abnormality in the offspring to environmental exposure of their parental line. This study also illustrated that oxidative stress and apoptosis appear to be a molecular component of the hepatocyte cell injury.

Exposure to low-dose bisphenol A induces spleen damage in a murine model: Potentially through oxidative stress?

“…A growing body of evidence indicates that exposure to environmental chemicals can cause serious detrimental effects on different body systems ( Camarca et al , 2016 ; Maamar et al , 2016 ; Al-Griw et al , 2017 ; Gassman, 2017 ). The endocrine-disrupting chemical BPA has specifically received increased attention due to its worldwide distribution with large exposure ( Camarca et al , 2016 ).…”

“…Environmental exposures to toxicants continue to be a major worldwide public health issue. A growing body of research has cautioned against the extensive use of environmental toxicants due to their longevity in the environment and their accumulation in the living tissues of organisms ( Camarca et al , 2016 ; Maamar et al , 2016 ; Al-Griw et al , 2017 ; Gassman, 2017 ). It is estimated that exposures cause approximately 24% of human abnormalities/diseases to toxicants, with the risk of abnormalities/diseases being passed on to future generations without direct exposure ( Hou et al , 2012 ).…”

Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A

“…Environmental toxicant exposure during the phase of germ cells, intrauterine, postnatal, and early lives has a significant impact on the phenotypes and vulnerability to diseases later in life ( Skinner et al , 2010 , 2013 ; Al-Gubory, 2014 ; Al-Griw et al , 2017 ). Endogenous hormonal control is disrupted by synthetic endocrine disruptors such as bisphenol A (BPA) ( Elobeid and Allison, 2008 ).…”

Therapeutic potential of vitamin D against bisphenol A-induced spleen injury in Swiss albino mice

“…There are increasing evidence that environmental exposures during intrauterine and postnatal periods or early life determine the phenotypic outcome and vulnerability to diseases in later life [1][2][3]. An endocrine disruptor, bisphenol A (BPA) has been used to produce epoxy resins and polycarbonate plastics [4].…”