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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
A subsequent study of renal clearance kinetics was also performed in a unilateral ureteric obstruction (UUO) model (Fig. 14.2C) [8]. In the UUO kidney, TXDC analysis showed that GS-AuNPs reached maximum accumulation in the renal cortex and medulla at 6.5 ± 4.2 min post-intravenous injection (p.i.). This time point was comparable to contralateral kidneys (5.2 ± 1.5 min) and sham kidneys (8.7 ± 3.4 min; Fig. 14.2G) [8]. Such an observation reveals no significant restriction for GS-AuNPs to reach the glomeruli from the bloodstream in the obstructed kidney [8]; however, both X-ray images and histological stains showed that most injected GS-AuNPs (1 h p.i.) were primarily deposited at the interface between the pelvis and medulla of the UUO kidney, while significantly fewer GS-AuNPs were observed in the contralateral kidney (Fig. 14.2D). A closer analysis shows that UUO-associated dilatation and atrophy of the medulla were observed (Fig. 14.2E). Meanwhile, the retained GS-AuNPs were found mainly in the normal tubular lumen and epithelial cells at the junction of the cortex and medulla within 8 days of p.i [8]. One of the most important findings of the authors’ study is that pathophysiological changes in the nephron can significantly slow down the transportation of renal-clearable AuNPs by altering their distribution pattern and the promoted cellular uptake of AuNPs by tubular cells.
Review of the Human Health Toxicology and Ecotoxicology of 1,4-Dioxane
Published in Thomas K.G. Mohr, William H. DiGuiseppi, Janet K. Anderson, James W. Hatton, Jeremy Bishop, Barrie Selcoe, William B. Kappleman, Environmental Investigation and Remediation, 2020
Janet K. Anderson, William B. Kappleman
In subchronic studies, doses of ≥185 mg/kg/day 1,4-dioxane administered to rats for 13 weeks in drinking water have been shown to cause adverse kidney effects. Male and female F344/DuCrj rats from the Kano et al. (2008) study had a significant increase in kidney histopathological alterations at doses of ≥657 mg/kg/day and ≥756 mg/kg/day for male and females respectively. Observed changes included reversible cellular swelling and vacuolar changes and nuclear enlargement of the proximal tubules (Kano et al., 2008). Significant increases in relative kidney weight were reported at lower doses of ≥274 and ≥185 mg/kg/day, respectively, in the male and female F344/DuCrj rats. Rats dosed for up to 34 days with the lethal dose of 1,428 mg/kg/day had vascular congestion in the kidneys and cell degeneration in the cortical epithelium (Fairley et al., 1934). Mice exposed to 2,916 mg/kg/day for up to 67 days had similar lesions (Fairley et al., 1934). The rats and mice exposed to 1,4-dioxane at 1,900 and 3,300 mg/kg/day, respectively, also exhibited non-neoplastic lesions in the renal cortex, including degeneration, necrosis, hemorrhages and vascular congestion, and kidney weight and size were increased (Fairley et al., 1934).
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
The Cd concentration in urine (CdU) has been proposed as an indirect biological indicator for Cd accumulation in the kidney. Several biomarkers for detecting nephrotoxic effects of Cd at different renal sites were studies in relation to CdU. In occupationally exposed males, the CdU thresholds for significant alterations of renal markers ranged, according to the marker, from 2.4 to 11.5 μg Cd/g creatinine. A threshold of 10 μg Cd/g creatinine (corresponding to 200 μg Cd/g renal cortex: the critical Cd concentration in the kidney) is confirmed for the occurrence of low-molecular-mass proteinuria (functional effect) and subsequence loss of renal filtration reserve capacity. In workers, microproteinuria was found reversible when reduction or cessation of exposure occurred timely when tubular damage was still mild (beta-2-microblobulinuria <1500 μg/g creatinine) and CdU had never exceeded 20 μg Cd/g creatinine. As the predictive significance of other renal changes (biochemical or cytotoxic) is still unknown, it seems prudent to recommend that occupational exposure to Cd should not allow that CdU exceeds 5 μg Cd/g creatinine.
Histopathological and inflammatory response in multiple organs of rats exposed to crack
Published in International Journal of Environmental Health Research, 2022
Daniel Souza, Barbara Rosarioa, Breno Casagrandea, Milena Viana, Debora Estadella, Rogerio Peres, Camilo Dias Seabra Pereira, Rogerio Peres
The histopathological evaluation showed that liver and kidney of rats presented morphological changes in both doses used (18 mg/kg and 36 mg/kg), with significant statistically differences (p < 0.05) in relation to control group, presenting several areas of coagulation necrosis in the liver parenchyma and renal cortex. In a previous published study, acute exposure (24 h) to crack cocaine (18 mg/kg) was not able to induce histopathological changes in liver and kidney of rats (Moretti et al. 2016). However, when the hepatotoxic potential of cocaine hydrochloride at different doses and periods of time was investigated, the administration of cocaine hydrochloride (50 mg/kg) induced glycogenic degeneration and steatosis (Shuster et al. 1977). When the dose of cocaine hydrochloride was increased to 100 mg/kg, extensive necrosis in liver was evident after 24 hours of exposure. At a dose of 50 mg/kg, a liver regeneration was detected after 3–5 days of administration (Shuster et al. 1977). In a study conducted by Powers et al. (1992), liver exposed to cocaine hydrochloride at doses of 10, 20 and 30 mg/kg (i.p.) for 5 days showed results similar to those of Shuster et al. (1977) in mice.
Carnosine in health and disease
Published in European Journal of Sport Science, 2019
Guilherme Giannini Artioli, Craig Sale, Rebecca Louise Jones
Carnosine, a histidine-containing dipeptide (HCD), is synthesised by bonding of the amino acids β-alanine and l-histidine, a reaction catalysed by carnosine synthase (Figure 1). Carnosine has been identified in vertebrates, including horses, greyhounds, camels and humans (see review by Boldyrev, Aldini, & Derave, 2013). Several animal species express other HCDs (anserine and ophidine/balenine), which are methylated forms of carnosine. Carnosine was, until recently, the only known HCD in human tissues, largely reported in skeletal and cardiac muscle, liver tissue and regions of the central nervous system. Peters et al. (2015) showed, however, that anserine is also expressed in the renal cortex of human kidney, in concentrations approximately two times higher than those of carnosine.
Renal damage induced by the pesticide methyl parathion in male Wistar rats
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Victor Hugo Fuentes-Delgado, María Consolación Martínez-Saldaña, María Luisa Rodríguez-Vázquez, Miguel Arturo Reyes-Romero, José Luis Reyes-Sánchez, Fernando Jaramillo-Juárez
The renal cortex of control rat kidney showed a normal cytoarchitecture. The cells of proximal tubular epithelium presented a positive PAS reaction on the basement membrane and on the microvilli of brush border membrane (Figure 5A). Also, 2 and 4 weeks after MP treatment, cells of proximal epithelium exhibited cytoplasmic vacuolization compatible with cellular edema (generalized cellular swelling), positive PAS inclusions, and brush edge loss in some segments (Figure 5B, C). At the sixth week of pesticide exposure, proximal cells displayed a decrease in cell edema and positive PAS inclusions (Figure 5D). Finally, 8 weeks after MP administration, both the re-establishment of tubular epithelium and cytoarchitecture of renal cortex were observed, showing similar characteristics with rats of the control group (Figure 5E).