Biomonitoring of the adverse effects induced by the chronic exposure to lead and cadmium on kidney function: Usefulness of alpha-glutathione S-transferase

2007 ◽  
Vol 377 (2-3) ◽  
pp. 165-172 ◽  
Author(s):  
Guillaume Garçon ◽  
Bruno Leleu ◽  
Thierry Marez ◽  
Farid Zerimech ◽  
Jean-Marie Haguenoer ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Kidney Function ◽  
Chronic Exposure ◽  
Glutathione S Transferase ◽  
Lead And Cadmium

The adverse effects of long-term l-carnitine supplementation on liver and kidney function in rats

2015 ◽  
Vol 34 (11) ◽  
pp. 1148-1161 ◽  
Author(s):  
L Liu ◽  
D-M Zhang ◽  
M-X Wang ◽  
C-Y Fan ◽  
F Zhou ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Kidney Function ◽  
Serum Alkaline Phosphatase ◽  
Lipid Synthesis ◽  
Inflammasome Activation ◽  
Carnitine Supplementation ◽  
Sprague Dawley ◽  
Reduced Body ◽  
Liver And Kidney

Levo-Carnitine (l-carnitine) is widely used in health and food. This study was to focus on the adverse effects of 8-week oral supplementation of l-carnitine (0.3 and 0.6 g/kg) in female and male Sprague Dawley rats. l-carnitine reduced body and fat weights, as well as serum, liver, and kidney lipid levels in rats. Simultaneously, hepatic fatty acid β-oxidation and lipid synthesis were disturbed in l-carnitine-fed rats. Moreover, l-carnitine accelerated reactive oxygen species production in serum and liver, thereby triggering hepatic NOD-like receptor 3 (NLRP3) inflammasome activation to elevate serum interleukin (IL)-1β and IL-18 levels in rats. Alteration of serum alkaline phosphatase levels further confirmed liver dysfunction in l-carnitine-fed rats. Additionally, l-carnitine may potentially disturb kidney function by altering renal protein levels of rat organic ion transporters. These observations may provide the caution information for the safety of long-term l-carnitine supplementation.

Adverse effects of pneumoperitoneum on renal function: involvement of the endothelin and nitric oxide systems

2008 ◽  
Vol 294 (3) ◽  
pp. R842-R850 ◽  
Author(s):  
Zaid Abassi ◽  
Bishara Bishara ◽  
Tony Karram ◽  
Samer Khatib ◽  
Joseph Winaver ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Adverse Effects ◽  
Renal Dysfunction ◽  
Kidney Function ◽  
Renal Plasma Flow ◽  
Abdominal Pressure ◽  
Oxide Systems ◽  
Excretory Function ◽  
Synthase Inhibitor

Increased intra-abdominal pressure (IAP) during laparoscopy adversely affects kidney function. The mechanism underlying this phenomenon is largely unknown. This study was designed to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO) systems in IAP-induced renal dysfunction. Rats were subjected to IAP of 14 mmHg for 1 h, followed by a deflation for 60 min (recovery). Four additional groups were pretreated with 1) ABT-627, an ETA antagonist; 2) A-192621, an ETB antagonist; 3) nitroglycerine; and 4) NG-nitro-l-arginine methyl ester, a NO synthase inhibitor, before IAP. Urine flow rate (V), absolute Na+ excretion (UNaV), glomerular filtration rate (GFR), and renal plasma flow (RPF) were determined. Significant reductions in kidney function and hemodynamics were observed when IAP was applied. V decreased from 8.1 ± 1.0 to 5.8 ± 0.5 μl/min, UNaV from 1.08 ± 0.31 to 0.43 ± 0.10 μeq/min, GFR from 1.84 ± 0.12 to 1.05 ± 0.06 ml/min (−46.9 ± 2.7% from baseline), and RPF from 8.62 ± 0.87 to 3.82 ± 0.16 ml/min (−54 ± 3.5% from baseline). When the animals were pretreated with either ABT-627 or A-192621, given alone or combined, the adverse effects of IAP on GFR, RPF, V, and UNaV were significantly augmented. When the animals were pretreated with nitroglycerine, the adverse effects of pneumoperitoneum on GFR and RPF were substantially improved. In contrast, pretreatment with NG-nitro-l-arginine methyl ester remarkably aggravated pneumoperitoneum-induced renal dysfunction. In conclusion, decreased renal excretory function and hypofiltration are induced by increased IAP. These effects are related to impairment of renal hemodynamics and could be partially ameliorated by pretreatment with nitroglycerine and aggravated by NO and ET blockade.

Adverse effects in kidney function, antioxidant systems and histopathology in rats receiving monosodium glutamate diet

2017 ◽  
Vol 69 (7) ◽  
pp. 547-556 ◽  
Author(s):  
María del Carmen Contini ◽  
Ana Fabro ◽  
Néstor Millen ◽  
Adriana Benmelej ◽  
Stella Mahieu
Keyword(s):  
Adverse Effects ◽  
Kidney Function ◽  
Monosodium Glutamate ◽  
Antioxidant Systems

scholarly journals S-Methyl Cysteine Protective Effects in Oreochromis Niloticus Fish Contaminated by Thiobencarb Herbicide

2020 ◽  
Author(s):  
Mostafa Ali Elmadawy ◽  
Walied Abdo ◽  
Amira Alaa El-Dein Omar ◽  
Nadia B. Mahfouz
Keyword(s):  
Adverse Effects ◽  
Histopathological Examination ◽  
Genotoxic Effect ◽  
Control Group ◽  
Protective Effects ◽  
Glutathione S Transferase ◽  
Commercial Feed ◽  
Significant Difference ◽  
Treated Fish

Thiobencarb which is a carbamate herbicide is used for managing undesirable weeds during rice cultivation in Egypt. This study was designed to investigate the adverse effects of a field dose of thiobencarb on Nile tilapia and ameliorating the role of the low dose of S-methyl cysteine (SMC). Experimental fishes were divided into four groups; first group was reared without any treatments and served as a control group; the second group was exposed to thiobencarb (36µg/L); the third group was fed on a commercial feed containing 200 mg of SMC/Kg in conjunction with thiobencarb added to aquarium (36µg/L) while, the fourth group was fed on a feed containing 200 mg of SMC/Kg only. Fishes were sacrificed at the end of the experimental course (two months) and sampling was carried out. Catalase, Glutathione S Transferase activities, Glutathione reduced, and Malondialdhyde levels were assayed. Genotoxic effect of thiobencarb and SMC on treated fish was investigated in erythrocytes, gills, and liver tissues using micronucleus and comet assay. Histopathological examination of livers, gills, and brain was also carried out. The results indicated that fish exposed to thiobencarb indicated herbicide dependent oxidative stress and genotoxic effect justified by a significant difference in antioxidant biomarkers as well as nuclear abnormalities and comet parameters compared to control values. Moreover, histopathological findings were in line with other results. SMC ameliorated the adverse effects which were effective in the improvement of DNA and oxidative damage in thiobencarb intoxicated fish.

scholarly journals Effect of Prenatal Exposure to Lead on Estrogen Action in the Prepubertal Rat Uterus

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Andrei N. Tchernitchin ◽  
Leonardo Gaete ◽  
Rodrigo Bustamante ◽  
Aracelly Báez
Keyword(s):  
Adverse Effects ◽  
Prenatal Exposure ◽  
Chronic Exposure ◽  
Cell Function ◽  
Environmental Pollutant ◽  
Striking Difference ◽  
Eosinophil Migration ◽  
Environmental Variations ◽  
Estrogen Stimulation

Lead is a widely spread environmental pollutant known to affect both male and female reproductive systems in humans and experimental animals and causes infertility and other adverse effects. The present paper investigated the effects of prenatal exposure to lead on different parameters of estrogen stimulation in the uterus of the prepubertal rat. In prenatally and perinatally exposed rats, estrogen-induced endometrial eosinophilia, endometrial stroma edema, and eosinophil migration towards the endometrium, and uterine luminal epithelial hypertrophy are enhanced while several other responses to estrogen appear unchanged. These effects may contribute to decrease in fertility following prenatal exposure to lead. The striking difference between most of these effects of prenatal exposure and the previously reported effects of chronic exposure to lead suggests that prenatal exposure to lead may neutralize the effects of chronic exposure to lead, providing partial protection of cell function against the adverse effects of chronic exposure to lead. We propose that the mechanism involved, named imprinting or cell programming, persisted through evolution as a nongenetic adaptive mechanism to provide protection against long-term environmental variations that otherwise may cause the extinction of species not displaying this kind of adaptation.

scholarly journals Evaluating the Role of the Steroid and Xenobiotic Receptor (SXR/PXR) in PCB-153 Metabolism and Protection against Associated Adverse Effects during Perinatal and Chronic Exposure in Mice

2020 ◽  
Vol 128 (4) ◽  
pp. 047011
Author(s):  
Riann Jenay Egusquiza ◽  
Maria Elena Ambrosio ◽  
Shuyi Gin Wang ◽  
Kaelen Marie Kay ◽  
Chunyun Zhang ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Chronic Exposure ◽  
Steroid And Xenobiotic Receptor ◽  
Xenobiotic Receptor

Searching for Perfect Marker - Differences and Dependencies in Serum Levels of Renalase, KIM-1, MCP-1, Calbindin and GST-Pi in Patients with Diabetes, Glomerulonephritis and Congenital Defects of the Kidney

2018 ◽  
Author(s):  
Natalia Maria Serwin ◽  
Magda Wiśniewska ◽  
Edyta Skwirczyńska ◽  
Karol Serwin ◽  
Oskar Wróblewski ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Function ◽  
Kidney Injury ◽  
Congenital Defects ◽  
Glutathione S Transferase ◽  
Kidney Toxicity ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Kidney Injury Molecule 1

Diagnosis of kidney diseases has recently become more comprehensive and accurate by using new renal markers. Despite the fact that creatinine and cystatin c have been sufficient in determining kidney function, they did not indicate the exact site of the damage and they were often insufficient in predicting the course of the disease. Aim of the study was to evaluate the potential correlations and differences in levels of six  factors related to kidney function and injury: kidney injury molecule-1 (KIM-1), ncalbindin (CALB), glutathione S-transferase Pi (GST-Pi), calbindin and monocyte chemoattractant protein-1 (MCP-1), between renal patients with diabetic nephropathy (DM), congenital defects (CD) of the kidney and glomerulonephritis (GN). Study involved 75 patients: 49 with diabetic nephropathy, 12 with congenital defects and 14 with glomerulonephritis. Levels of renalase was measured using immunoenzymatic tests. Levels of other markers: calbindin, glutathione-S-transferase (GST-pi), interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1) and monocyte chemoattractant protein-1 (MCP-1), were analyzed using Kidney Toxicity-1 Panel and BioPlex system, designed for analyses in urine and optimized by us for serum.From all analyzed markers, only levels of KIM-1 differed significantly between any subgroups, and that was for CD and DM. Renalase correlated significantly negatively with creatinine and positively with all other markers, apart from MCP-1. Obtained results indicate, that serum renalase, KIM-1, calbindin and GST-pi are related to kidney function, with KIM-1 being the most exact, while MCP-1 levels are unrelated to creatinine and glucose levels, does not differ between patients with diabetic nephropathy and other subgroups, and therefore seem to be independent of diabetes. Also, serum-optimized Kidney Toxicity Panel 1 kit for determination of selected markers gave results similar to previous ones and therefore the method can be valuable in determination of analyzed factors.

Sign in / Sign up

Export Citation Format

Share Document