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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.
Disposition of methylmercury over time in a 75% nephrectomized rat model
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Sarah E. Orr, Lucy Joshee, Jennifer Barkin, Christy C. Bridges
Renal accumulation of mercuric ions was shown to occur within the first hour of exposure (Zalups 1993). The present data also suggest that renal accumulation of MeHg is rapid. Further, it appears that renal accumulation of MeHg continues over the 3-day exposure period. This accumulation might be associated with binding of mercuric ions to intracellular thiols after uptake into cells. Retention of mercuric ions within renal tubular cells may lead to injury and acute tubular necrosis. Interestingly, treatment of animals with MeHg over the course of 3 d led to a significant rise in urine volume. Indeed, renal tubular injury is characterized by the presence of polyuria. Current measurements of plasma creatinine support the observations that renal accumulation of MeHg leads to tubular injury. After 1-day treatment, levels of plasma creatinine in controls (Group 1) increased 3.4-fold while there was no significant change in corresponding NPX animals (Group 2). It is important to note that the accumulation of MeHg was higher in control kidneys, suggesting that during the initial period of exposure, control kidneys may be at greater risk of MeHg-induced intoxication. After 2 d treatment with MeHg, plasma creatinine in controls (Group 3) was elevated by only 30%, suggesting that the initial period of exposure led to the most significant injury in these animals. In corresponding NPX rats (Group 4), 2 d of exposure led to an 80% increase in plasma creatinine, suggesting that as MeHg accumulation in the remnant kidney rises, the nephrons become more susceptible to MeHg-induced renal injury. The delay in tubular injury may also be related to the concomitant reduction in renal blood flow to NPX kidneys.