Abstract
Lead and di-(2-ethylhexyl) phthalate (DEHP) are common environmental toxicants of concern around the world. Although effects of individual exposures to both agents are well documented, there is a dearth of information on the effects of co-exposure to both agents. In this study, combined exposure to lead and DEHP was investigated for effects on ATPase activities in the liver, brain and kidney tissues of rats. Male albino rats were daily exposed to either 200 ppm lead as lead acetate in their drinking water and/or 100 mg DEHP kg-1 body weight in olive oil by gastric intubation for 30 days. Changes in total body weight, relative organ weights as well as brain, hepatic and renal activities of total, Na+K+ -, Ca2+ - and Mg2+-ATPases were used as biomarkers of toxicity. Hepatomegaly and brain atrophy heralded exposure to both agents. Individual exposure to lead and DEHP resulted in reduction in hepatic Ca2+- and Mg2+- ATPase activities but no significant effect on total ATPase activity, however combined exposure produced significant activation of Ca2+-, Na+K+- and total ATPase while restoring Mg2+ - ATPase towards control. A potentiating effect on lead by DEHP was observed in hepatic Na+K+ - ATPase. Lead stimulated the activities of renal Ca2+- and total ATPases while DEHP on the contrary caused significant reduction in total ATPase activity and no significant effects on Ca2+- ATPase activity. Co-treatment produced antagonistic effects leading to normal renal Ca2+- and total ATPase activities. Brain Na+K+ -, Ca2+ - and total ATPase activities were depressed in co-exposure while Mg2+ - ATPase was up-regulated. Lead potentiated DEHP-induced inhibition of brain total - ATPase while co-treatment produced antagonistic effects on brain Ca2+ - ATPase. The findings of this study highlight organ specific variations in response to combined lead and DEHP exposure in rats. Key words: Hepatotoxic, neurotoxic, ATPases, DEHP, lead, co-exposure, hepatomegaly.
Highlights
Despite the global move to phase out leaded-gasoline, lead has persisted as an environmental pollutant of grave concern with its deleterious effects felt among children (Nriagu et al, 1996)
The DEHP-exposed rats displayed reduced appetite throughout the study compared to animals in the other groups and this might account for their weight loss
It was observed that Pb antagonized DEHP - induced decrease in bodyweight in this study, and mechanisms that may be compensatory led to the highest increase in total body weight in this co-treated group
Summary
Despite the global move to phase out leaded-gasoline, lead has persisted as an environmental pollutant of grave concern with its deleterious effects felt among children (Nriagu et al, 1996). Several studies have shown that lead is ubiquitous in the environment (Ademuyiwa et al, 2002; Adeniyi and Anetor, 1999) and causes oxidative stress in the body by interacting with glutathione, a known natural antioxidant in the body (Jangid et al, 2016). Glutathione is a tripeptide consisting of γ-glutamic acid, cysteine and glycine It is found in several tissues (Kosnet et al, 1998) and lead’s interaction with glutathione leads to replacement of the hydrogen on two sulphydryl groups on adjacent molecules by lead. The strong bond that results effectively eliminates the two glutathione molecules from further reaction thereby eliciting all the conditions that arise as a result of oxidative stress, such as diabetes, nervous system disorders, cardiovascular diseases, aging, cancer etc (Ademuyiwa et al, 2005; 2007; Dosumu et al, 2005)
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