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Occupational toxicology of the kidney
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
The proximal tubule is the most common site of chemically induced injury, including injury from heavy metals, antibiotics, hydrocarbons, herbicides, and organic solvents. The type of injury is dependent on the conditions of exposure (dose and duration) and the properties of the toxicant. Acute injury generally results in tubular epithelial necrosis that may be reversible by epithelial regeneration, depending on the severity of the insult and persistence of the compound. Chronic injury presents as tubulointerstitial nephritis that is often irreversible and can progress to renal failure.
Development of Regulations for Radionuclides in Drinking Water
Published in Barbara Graves, Radon, Radium, and Other Radioactivity in Ground Water, 2020
The primary chemical toxic effect of natural uranium is on the kidneys. This has been seen from evidence for over a century from both medical administration to humans and numerous animal studies. Nephritis (inflammation of the kidneys) and changes in urine consumption are clear symptoms. Based on this evidence, the Adjusted Acceptable Daily Intake for uranium is 60 micrograms per liter and is computed by allocation of the Acceptable Daily Intake for a 70-kg adult consuming two liters of water per day. This level is roughly equivalent to 40 pCi/L.
National Primary Drinking Water Regulations for Radionuclides
Published in Edward J. Calabrese, Charles E. Gilbert, Harris Pastides, Safe Drinking Water Act, 2017
As evidenced by over a century of data from both medical administration to humans as well as from numerous animal studies, the primary chemical toxic effect of natural uranium is on the kidneys. Nephritis (inflammation of the kidneys) and polyuria (excessive urine excretion) are clear symptoms. It is estimated by EPA that health effects to the kidney are of the same order of magnitude as radiotoxic effects to bone.
Serum miRNA-146a and vitamin D values in chronic renal ailment with and without comorbid cardiovascular disease
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Fatma K. A. Hamid, Alshaymaa M. Alhabibi, Mona A. Mohamed, Hanaa Hussein El-Sayed, Nehad Rafaat Ibrahim, Ghadir Mohamed Hassan Elsawy, Entsar M. Ahmad
The present results support those of Aguado-Fraile et al. [36], who showed the value of serum miR-146a as a diagnostic biomarker of acute kidney injury capable of detecting patients at an early stage of the disease. According to Perez-Hernandez et al. [37], renal fibrosis brought on by lupus nephritis is associated with urine levels of miR-146a. According to a theory put up by Morishita et al. [38], miR-146a lowers renal fibrosis by obstructing pro-inflammatory and pro-fibrotic signaling pathways. CKD patients who had CVD complications had significantly higher blood levels of miR-146a, compared to the control group, but there was no statistically significant difference in miR-146a levels as compared to CKD patients. As a result, serum miR-146a levels seem to be of limited value in identifying CVD. High blood miR146a levels, which are elevated by coronary artery disease, have been linked to an independent prediction of cardiac events, according to Takahashi and colleagues [39]. This is consistent with the findings of Raitoharju et al. [40], who found that atherosclerotic artery tissues had higher levels of miR-146a than non-atherosclerotic artery tissues did.
Thymol Reduces Hepatorenal Oxidative Stress, Inflammation and Caspase-3#xd; Activation in Rats Exposed to Indomethacin
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Tijani Abiola Stephanie, Olori O. David, Ebenezer O. Farombi
Drug-induced multi-organ toxicities are common adverse reaction triggered by numerous drugs like indomethacin (IND). Indomethacin is one of the non-steroidal anti-inflammatory drugs used as analgesic and also has antipyretic property. However, its adverse side effects have raised a lot of concern for its continuous use in clinical settings. Indomethacin cause many organ toxicities including liver, kidney and gastrointestinal toxicities in humans and experimental animals [1,2]. In the liver, IND has been associated with hepatocellular enzymes elevation and cholestatic jaundice whereas in the kidney, IND caused acute interstitial nephritis typified by wide spread interstitial edema with infiltration of inflammatory cells [3,4]. The mechanisms by which IND causes its toxicities include prostaglandin synthesis inhibition, generation of reactive oxygen species (ROS) resulting to cellular oxidative stress, inflammation and apoptosis [5].
Cylindrospermopsin toxicity in mice following a 90-d oral exposure
Published in Journal of Toxicology and Environmental Health, Part A, 2018
N. Chernoff, D.J. Hill, I. Chorus, D.L. Diggs, H. Huang, D. King, J.R. Lang, T.-T. Le, J.E. Schmid, G.S. Travlos, E.M. Whitley, R.E. Wilson, C.R. Wood
In mouse, the possibility of a toxicity being initiated by toxins produced by cyanobacteria in the reservoir was tested using a variety of cultures of cyanobacterial species present in the reservoir. Freeze-dried cultures of Cylindrospermopsis raciborskii administered intraperitoneally in mice produced hepatic necrosis and adverse effects in a variety of other organs (Hawkins et al. 1985). CYN was isolated (Ohtani, Moore, and Runnegar 2002), the alkaloid considered to be the primary toxin produced by C. raciborskii, and in subsequent years, evidence indicated that both lyophilate extracts of CYN-containing cyanobacteria and purified CYN induced a spectrum of adverse effects in mice that were similar to those seen in the affected human population. Hepatic toxicity was characterized by changes in levels of serum enzymes that are indicative of hepatic injury as well as histopathology, demonstrating varying degrees of centrilobular injury (Chernoff et al. 2010, 2014; Harada et al. 1994; Hawkins et al. 1985; Zurawell et al. 2005). Renal effects that were observed included interstitial nephritis and/or tubular epithelial necrosis (Falconer et al. 1999; Hawkins et al. 1985). Other adverse effects included CYN-induced bleeding in the gastrointestinal tract (GIT) (Chernoff et al. 2010; Hawkins et al. 1985; Seawright et al. 1999), lungs (Bernard et al. 2003; Hawkins et al. 1985), heart (Hawkins et al. 1985; Seawright et al. 1999), and periorbital sinus and tail tips (Chernoff et al. 2010; Rogers et al. 2007; Shaw et al. 2000).