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Toxicology of CERCLA Hazardous Substances
Published in Barry L. Johnson, Impact of Hazardous Waste on Human Health, 2020
Many substances are known to be toxic to the kidneys, causing nephrotoxicity. Several metals, notably cadmium, chromium, lead and mercury, and chlorinated hydrocarbon compounds like carbon tetrachloride and chloroform are particularly nephrotoxic, causing severe damage to the tubules. The effect is to impair the removal of wastes from the body, an outcome that can be fatal.
Toxicity of organic solvents
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
For solvent exposure, the first point is important. Exposure to some chemicals will cause damage to the kidney (nephrotoxicity), which may in turn jeopardise excretory efficiency. This may be seen as a poorer ability of the body to excrete toxicants and their breakdown products or the inability of the body to retain chemicals that it needs (such as glucose, albumin and amino acids).
Macrophage Targeting: A Promising Strategy for Delivery of Chemotherapeutics in Leishmaniasis and Other Visceral Diseases
Published in Sarwar Beg, Mahfoozur Rahman, Md. Abul Barkat, Farhan J. Ahmad, Nanomedicine for the Treatment of Disease, 2019
Jaya Gopal Meher, Pankaj K. Singh, Yuvraj Singh, Mohini Chaurasia, Anita Singh, Manish K. Chourasia
Anti-leishmanial drugs are known to become infective against the causative pathogens. So their delivery in a very specific and targeted manner is highly required to circumvent the current issues. Novel techniques for the delivery of anti-leishmanial drugs via liposomes, nanoparticles, and other carrier systems have been developed and are found to be suitable in treatment of leishmaniasis in cell lines and animal models. Macrophage targeting of these drugs are also investigated by researchers in order to enhance the therapeutic potential. Amphotericin Bis the standard gold drug for treatment of visceral leishmaniasis and it is commercially available as both conventional and novel drug delivery based formulations. The novel formulations were claimed to reduce its well-known side effect: nephrotoxicity. However, there is controversy on these aspects whether there is a significant reduction in the toxicity associated with amphotericin B in its commercial formulations. Apart from the toxicity issues, the stability of formulations and their augmentation in efficacy has been challenged. Our research group have been working on novel drug delivery of anti-leishmanial drugs, and we have reported some promising delivery tools for treatment of leishmaniasis. We have developed a novel formulation of amphotericin B, i.e., chitosan polymer based nanocapsule by employing polymer deposition technique. The developed nanocapsule was stable, and chitosan was found to stabilize the formulation against any stress. In vitro toxicity study in J774A.1, cell line and erythrocytes showed the formulation to be comparatively less toxic than the marketed formulations. In-vitro anti-leishmanial activity study revealed very lower IC50 by the nanocapsules in macrophage-amastigote system. Our developed formulation exhibited higher in vitro internalization in macrophages that the plain drug. Further nanocapsules containing amphotericin B were evaluated in hamsters infected with L. donovani, and a very encouraging result (86.1% ± 2.08% parasite inhibition) was seen. To understand the molecular activities for such experimental findings, RT-PCR was employed, and the quantitative mRNA analysis was performed. Results suggested that there was up-regulation of TNF-α, IL–12, and nitric oxide synthase whereas TGF-β, IL–10, and IL–4 were down-regulated. The overall research findings put forward that our developed amphotericin B bearing nano-capsules could perform well against leishmaniasis and can be further explored for other pre-clinical and clinical investigations (Asthana et al., 2013).
Fagonia indica ameliorates chromium-induced nephrotoxicity: Role of antioxidant activity and pro-inflammatory cytokines in in-vivo renoprotection
Published in Archives of Environmental & Occupational Health, 2023
Eman A. A. Abdallah, Abdullah Almilaibary, Mohamed F. El-Refaei
Nephrotoxicity is the term used to describe a significant reduction in kidney function caused by the toxic effects of medicines and other substances, and it can occur due to different factors, including crystal nephropathy, thrombotic microangiopathy, inflammation, and renal tubular toxicity.45,46 Cr is recorded as the most toxic and hazardous metal ion found in soil and water. Mostly, Cr toxicity is caused by oxidative stress, which results in the creation of ROS in the cells, negatively altering the cellular signaling pathways and consequently inducing mitochondrial dysfunction due to the rapid activation of NF-κB, STAT3, and other proteins that encourage gene expression during an inflammatory response.47 Clinical studies show that stomach cancer among workers (gold miners) was caused by Cr oral toxicity in some individuals.48 Furthermore, women who worked in Cr plating are confronting acute hepatitis with jaundice and exhibiting mild to moderate liver complications.49
Pesticide-induced changes in cholinesterase activity and chronic kidney disease of unknown etiology among farmers in Nakhon Ratchasima, Thailand
Published in Human and Ecological Risk Assessment: An International Journal, 2021
Ekarat Sombatsawat, Dana Boyd Barr, Parinya Panuwet, Mark Gregory Robson, Wattasit Siriwong
Previous studies have provided strong evidence that pesticides can cause damage to many tissues and organs, including the kidneys (Jamal et al. 2016). Several studies have demonstrated the nephrotoxic effects of pesticides based on research in laboratory animals (El-Bini Dhouib et al. 2015; Kaya et al. 2018). According to previous research, accumulation of pesticides in kidney tubular cells could increase levels of reactive oxygen species which subsequently induced proximal tubule injury (Mølck and Friis 1997). Nephrotoxicity can be detected by a change in renal function as assessed by the glomerular filtration rate (GFR), serum creatinine (SCr), or urinary output (Barnett and Cummings 2018). Although knowledge of the pathogenesis of kidney injury from OP and carbamate poisoning is limited, the suggested mechanisms include BuChE activity in the renal distal convoluted tubule and an increase in oxidative stress (Mamoulakis et al. 2017; Tsarouhas et al. 2018). In cases of OP and carbamate poisoning, the progression from nephropathy to chronic renal insufficiency (Ghosh et al. 2018) and premature death (Ramirez-Rubio et al. 2013) is generally undetected, as renal damage occurs gradually.