Delayed biochemical changes induced by mercury intoxication are prevented by zinc pre-exposure

Abstract

This work evaluated the delayed effects of mercury and the effectiveness of zinc in preventing such effects. Pups were pre-treated with 1 daily dose of ZnCl(2) (27 mg/kg/day, by subcutaneous injections) from 3rd to 7th postnatal day and received 1 daily dose of 5 mg/kg of HgCl(2), for 5 subsequent days (8-12 days old). Animals were euthanized 21 days after the end of Hg-exposure. Porphobilinogen-synthase activity as well as zinc and mercury contents was determined in the liver and kidneys. Alanine aminotransferase, aspartate aminotransferase and lactic dehydrogenase activities as well as urea, creatinine and glucose levels were analyzed in plasma or serum. Some animals were considered more sensitive to mercury, since they did not recover the body weight gain and presented an increase of renal and hepatic mercury content, urea and creatinine levels; a decrease in renal porphobilinogen-synthase and alanine aminotransferase activities, as well as a decrease in the liver and an increase in kidney weights. Some animals were considered less sensitive to mercury because they recovered the body weight and presented no biochemical alterations in spite of mercury in the tissues. Zinc prevents partially or totally the alterations caused by mercury even those that persisted for a long time after the end of exposure. These findings suggest that there is difference among the animals regarding the sensitivity to mercury.

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

“…However, recent studies have shown that zinc can be used as an important treatment against several toxicants, such as toxic metals. In line with this, previous studies from our group demonstrated that zinc acts as a protector agent against several mercury toxic effects in rats (Franciscato et al, 2011;Peixoto et al, 2003).…”

Ameliorative effects of hydroalcoholic extract of Lavandula officinalis L. on cyclophosphamide-induced nephrotoxicity in mice

“…Our results were parallel to some studies which indicated, the after CP intoxication, significant depletion of the GSH level and also significant increases in MDA, BUN and Cr was evidenced, corroborating the state of oxidative stress (39)(40)(41)(42). The human body is equipped with possesses defense systems against free-radical damage like the nonenzymatic antioxidants such as reduced GSH (41) and endogenous antioxidant enzymes such as GPx, SOD and CAT (43). Hence, generation of high levels of ROS or any disturbance in the oxidantantioxidant status can result in oxidative damage to macro molecules (DNA, proteins and lipids), tissues or organs (44).…”

The Hepatoprotective Effect of Gallic Acid on Mercuric Chloride-Induced Liver Damage in Rats

“…The induced oxidative stress due to ROS may lead to the initiation and progression of some diseases, such as cardiovascular diseases, diabetes, and neurodegenerative disorders (38). The human body is equipped with defense mechanisms against free-radical damage, induced by nonenzymatic antioxidants (eg, GSH) (20) and endogenous antioxidant enzymes (eg, GPx, SOD, and CAT) (41). Therefore, high levels of ROS or any disturbance in the oxidant-antioxidant status can result in oxidative damage to macromolecules (eg, DNAs, proteins, and lipids), tissues, or organs (42).…”