Experimental research Concomitant protective and therapeutic role of verapamil in chronic mercury induced nephrotoxicity in the adult rat: histological, morphometric and ultrastructural study

Abstract

IntroductionMercury intoxication is a widespread problem as mercury is used in the manufacture of thermometers, batteries and electrical switches. It forms one of the most diffusible environmental pollutants. Mercury has a nephrotoxic effect which could occur at low exposure levels. Verapamil could help in the treatment of mercuric toxicity. The aim of the study was to examine the protective and therapeutic effect of concomitant verapamil on chronic mercuric chloride nephrotoxicity. This was done through histological, morphometric and transmission electron microscopic studies.Material and methodsSixty adult male albino rats were used. The rats were divided into a control group and 4 experimental groups: group I (HgCl2), group II (concomitant HgCl2 and verapamil), group III (HgCl2 withdrawal) and group IV (HgCl2 withdrawal then verapamil treatment).ResultsChronic administration of HgCl2 resulted in cortical nephrotoxic effects in the form of glomerular sclerosis, acute tubular necrosis and interstitial inflammatory cellular infiltration which eventually ended in interstitial fibrosis. Concomitant use of verapamil with HgCl2 improved the previous pathological changes partially. The findings in group III were less severe compared to group IV. The persistence of the pathological findings in these groups reflects the irreversible nephrotoxic changes caused by chronic HgCl2 exposure.ConclusionsWe concluded that the concomitant administration of verapamil has a much better effect in minimizing the nephrotoxic effect caused by chronic HgCl2 than its therapeutic administration. So, we recommended the prophylactic use of verapamil in suspected cases of chronic mercuric chloride nephrotoxicity to preserve renal function.

Mercuric Chloride Induced Nephrotoxicity: Ameliorative Effect of Carica papaya Leaves Confirmed by Histopathology, Immunohistochemistry, and Gene Expression Studies

“…In contrast, the kidneys of HgCl 2 -treated rats showed morphological changes in kidney tissues such as glomerular congestion, tubular vacuolization, glomerular atrophy, interstitial inflammation, disorganization of Bowman’s capsules, and parietal layer adhesion. These findings are consistent with previous studies done by Haleem et al (2015), Elshemy et al (2018), and Vervaet et al (2017) on mercuric chloride and heavy metal intoxication. − Recently, a scientific investigation was carried out on human renal tissues containing heavy metal, which was stained with Masson’s trichrome. The findings revealed the appearance of blue color around the cell margin and dark brown color in the nucleus, indicating the fibrotic and molecular changes in the glomerulus and renal tubules due to toxin deposition …”

“…These findings are consistent with previous studies done by Haleem et al (2015), Elshemy et al (2018), and Vervaet et al (2017) on mercuric chloride and heavy metal intoxication. 82 − 84 Recently, a scientific investigation was carried out on human renal tissues containing heavy metal, which was stained with Masson’s trichrome. The findings revealed the appearance of blue color around the cell margin and dark brown color in the nucleus, indicating the fibrotic and molecular changes in the glomerulus and renal tubules due to toxin deposition.…”

The role of vitamin E in the prevention of zoledronic acid-induced nephrotoxicity in rats: a light and electron microscopy study

“…Vitamin E (Vit E – α-tocopherol), as a fat-soluble antioxidant, stops the production of reactive oxygen species formed when fat undergoes oxidation, and is incorporated into cell membranes to protect against oxidative damage [ 9 ]. Like verapamil and selenium, Vit E is being studied for its antioxidative effects in the kidney [ 10 , 11 ].…”

CDP‐choline circumvents mercury‐induced mitochondrial damage and renal dysfunction

“…It is recognized that the accumulation of Hg 2þ in kidney tissue induces cortical nephrotoxicity effects characterized by tubular necrosis, glomerular sclerosis, and infiltration of interstitial inflammatory cells, which lead to renal dysfunction (Ambudkar et al, 1988;Haleem et al, 2015). In mitochondria, Hg 2þ induces oxidative phosphorylation failure and membrane permeability transition from selective to non-selective (Southard and Nitisewojo, 1987;Ambudkar et al, 1988).…”