INTRODUCTION: Chlorpyrifos is one of the most commonly used organophosphates in agriculture. Report on animal models of chronically exposed chlorpyrifos showed significant histo-structural renal damage. Moreover, evidence of high incidence of diabetes mellitus were observed among agricultural workers exposed to organophosphates. Available evidence linking derangement of glucose metabolism pathway with renal damage in this chronically exposed chlorpyrifos is lacking. The aim of this study was to determine the involvement of advanced glycation end-products formation in the development of nephrotoxicity in animals with chronic subcutaneous exposure to chlorpyrifos. MATERIALS AND METHODS: Eighteen rats were divided into three groups, with six rats in each group. Group 1 served as a control group, while Groups 2 and 3 received subcutaneous 3% dimethyl sulfoxide and 97% volume per volume soy oil as a vehicle or chlorpyrifos, respectively, alternate day for 180 days. Blood samples were taken for biochemical analysis. Kidney tissues were examined for immunohistochemistry and gene expression of pathways related to oxidative stress and advanced glycation end-products. RESULTS: Serum fasting glucose, creatinine, advanced glycation end-products and malondialdehyde levels were significantly increased (p<0.05), whereas paraoxonase-1 level was decreased in chlorpyrifos-treated rats compared with the control groups (p<0.05). The proximal tubular cells and the glomeruli of chlorpyrifos-exposed kidney showed strong malondialdehyde and advanced glycation end-products expression respectively. Gene expression of catalase and glutathione reductase were downregulated in the chlorpyrifos-treated rats. CONCLUSION: Glucose derangement and oxidative stress are the possible mechanisms of organophosphate-induced kidney damage.
INTRODUCTION: Exposure to environmental arsenic remains a major public health challenge. Human is exposed to arsenic from groundwater as a result of anthropogenic activities. Chronic exposure to inorganic arsenic has been linked with multiple medical conditions. Therefore, many agricultural countries have shifted the use of inorganic to the organic-based herbicide, monosodium methylarsonate (MSMA). However, with increasing numbers of chronic kidney disease of unknown etiology (CKDu), chronic exposure to herbicide is believed as one of the potential explanations. To date, studies on chronic effects of organic arsenic on the kidney are limited. Therefore, this study aimed to investigate the effect of chronic oral organic arsenic exposure on the rat’s kidney. MATERIALS AND METHOD: Thirty-six Sprague Dawley rats were randomly divided into treatment and its corresponding control groups according to the duration of observations either 2, 4 or 6 months. Both groups were subdivided into three subgroups, each with six animals per subgroup. The treatment groups were given oral MSMA at 63.20 mg/kg body weight, while control groups received distilled water. At the end of each duration, blood was collected for the renal profile, urine for neutrophil gelatinase-associated lipocalin (NGAL) marker, and kidney tissues were harvested for arsenic level measurement and histological analysis. RESULTS:Arsenic level and urinary NGAL were higher in all treatment groups than its corresponding control groups. Histological findings showed progressive pathological changes in the glomeruli and proximal tubules. CONCLUSIONS:Chronic oral exposure to low dose organic arsenic has demonstrated evidence of kidney injury in rats.
Introduction: An increased incidence of chronic kidney disease (CKD) was reported among agricultural workers who were exposed to organophosphates (OP). There is little information on the effects of chronic low OP exposure on kidney in experimental animals. Chlorpyrifos (CPF) is a common type of OP used in agriculture. Thus, the aim of this study was to assess the effects of chronic low subcutaneous exposure of CPF on the kidney. Methods. Eighteen male Sprague Dawley rats were divided into three groups, with six rats in each group. Group 1 served as a control group, and groups 2 and 3 received a subcutaneous vehicle (3% dimethyl sulfoxide + 97% v/v soy oil) or CPF (18.0 mg/kg) respectively, every other day for 180 days. Serum urea, creatinine, uric acid, cystatin C, electrolyte levels, acetylcholinesterase (AChE), and arylesterase (ArE) activities were measured. Histopathological changes in the kidney tissues were examined. Results. Urea, creatinine, uric acid, and cystatin C levels were significantly increased (p < 0.05), while electrolytes were reduced (p < 0.05) in the CPF-treated rats. Both AChE and ArE activities were depressed in the CPF group (p < 0.01 and p < 0.001, respectively). Diffuse necrosis of proximal tubules and glomerular hypercellularity were observed in the kidney in the CPF group. Conclusion. A chronic low dose of CPF via subcutaneous exposure caused considerable renal tubular necrosis and derangement of glomerular function. These findings suggest that chronic occupational OPs exposure can cause kidney damage.
Introduction: Monosodium methylarsonate (MSMA) is an organic arsenical pesticide widely used in agriculture. Humans are exposed to arsenic through drinking water and anthropogenic activities. Exposure to inorganic arsenic has been linked with multiple health problems. However, studies focusing on chronic organic arsenic exposure and its adverse effects on kidney were limited. The purpose of current study was to determine the effects of chronic organic arsenic exposure in rats kidney by light and electron microscopy. Materials and Method: Thirty-six male SpragueDawley rats were divided into six groups (n=6); three control and three treatment group respectively. All the control group was given distilled water via oral gavage. The treatment group was given oral gavage of MSMA at 42.10 mg/kg body weight (BW) which is equivalent 1/30 LD50 of MSMA. The control and treatment groups were sacrificed at two month, four month and six months interval. Both kidneys harvested for light microscopy and electron microscopy study. Results: Showed progressive changes. The changes initially focal and became diffused involving glomerular; such as glomerular hypercellularity, glomerular shrinkage and dilated Bowman's space. Meanwhile, in proximal tubules, showed diminished brush borders, detachment of nucleus and basement membrane thickening. Electron microscopy showed flattened cell bodies of podocytes, effacement and fusion of podocytes foot processes, thickening of glomerular basement membrane, and discontinuity of brush border. The control and two-months treated group appeared to be normal. Conclusion: Chronic organic arsenic (MSMA) exposure induced chronic kidney injury.
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