Human Impacts on Nitrite Levels in the Ecosystem
1. Numerous human impacts, such as anthropogenic as well as the administration of nitrogenous fertilizers to increase agriculture returns and improper waste management have considerably increased the quantity of nitrite accessible in the ecosystem. Water supply has also been reported to have greater nitrite contents compared to the recommended level. Exposure to NaNO2, on the other hand, has been associated with a variety of illnesses, including birth deformities, neurological damage, respiratory system dysfunction, oxidative stress, as well as carcinogenicity along mutagenicity. Because of the aforementioned factors, human exposure to NaNO2 is nearly unavoidable; hence, the health risks associated with NaNO2 may be inevitable. The kidney is among the organ that is most sensitive to external poisons. Following that, nephrotoxicity induced by NaNO2 has already been linked to enhanced fibrotic, inflammation, mitochondrial damage, as well as stress indicators across rat models, along with higher creatinine and urea, along with greater renal filtration rate throughout human subjects. In addition to various renal function indicators, the concentrations of the adenosine deaminase (ADA), a significant enzyme found inside the kidney, including arginase that catalyzes the creation of urea plus ornithine from arginine, could be evaluated to measure kidney activity. Higher urea level is also associated with increasing arginase action. As a result, regulating ADA along with arginase activity could be a therapeutic method for dealing with kidney biomarker changes. As a result, any natural substance, which may control the activity of these enzymes, might be a viable nephrotoxicity preventative. The present study looked at the effects of curcumin (20 mg/kg body weight/day) upon arginase as well as ADA functions, along with other renal indicators including oxidative stress markers, using Wistar rats subjected to sodium nitrite (NaNO2) (60 mg/kg body weight, single dose) throughout 28 days. These analyses indicate that the rats subjected to NaNO2 had drastically changed ADA, arginase, as well as other indicators of renal function, along with oxidative stress. Curcumin pretreatment, on the other hand, dramatically reduced the changed ADA as well as arginase activity, along with other metrics. These findings imply that modest curcumin consumption at an appropriate daily dose may reduce food-induced kidney injury by regulating ADA as well as arginase activity, enhancing the antioxidant system, and suppressing lipid peroxidation.
2. The finding of this study can be supported by other relevant studies. According to an original study on rats, Akinyemi et al (2017) mention Curcumin inhibited ADA as well as arginase functions while boosting endothelial nitric oxide (NO) as well as functioning SH groups throughout the kidney, reducing cadmium (Cd)-induced nephro oxidative damage. Curcumin also prevents Cd buildup in the kidney, most likely owing to its chelating properties. As a result, these actions point to several possible modes of action underlying their renoprotective effects. Curcumin co-treatment with 12.5 mg/kg as well as 25 mg/kg enhances nonenzymatic antioxidant capacity along with NO inside the kidney, while simultaneously lowering malondialdehyde concentrations as well as renal indicators. Hence, finding from Akinyemi et al (2017) suggest Curcumin is effective enough to reduce ADA and arginine.
According to another study on rats, Longobardi et al (2021) mention Curcumin (CURC) seems to be an anti-apoptotic, anti-inflammatory, as well as antioxidant polyphenol found in turmeric. Through controlling inflammation, lowering NO levels, as well as decreasing oxidative DNA damage within kidney as well as liver cells, the co-treatment of Ochratoxin A (OTA) + CURC mitigated the negative impact of chronic OTA therapy. Histopathology demonstrated that OTA + CURC therapy causes an Iba1+ macrophagic invasion inside the cells, with fewer CD3+ T-lymphocytes. Finally, researchers found that CURC had cytoprotective as well as antioxidant effects in rats when they were exposed to OTA. Hence, the findings from this study can also suggest the antioxidant role of Curcumin.
3. Orr & Bridges (2017) mention mercury; lead, cadmium, as well as arsenic are some of the most dangerous environmental toxins. Interaction with one or all of such elements is inevitable since they are ubiquitous throughout the ecosystem. All of these metals can cause Chronic kidney disease (CKD), leading to nephrotoxicity. Therefore, to prevent these from happening, curcumin can be used. Turmeric, as well as curcumin’s active components, offers the widest range of ethnomedicinal as well as biological effects, comprising anticarcinogenic, antioxidative, antibacterial, anti-inflammatory, along antifungal activity. Curcumin has been shown to have therapeutic benefits in animal models involving cadmium-induced kidney damage including oxidative stress (Akinyemi et al., 2017). Therefore, a novel therapeutic approach using Curcumin can help to reduce the chance of nephrotoxicity caused by environmental and industrial toxicants.
References
Adewale, O. O., Bakare, M. I., & Adetunji, J. B. (2021). Mechanism underlying nephroprotective property of curcumin against sodium nitrite?induced nephrotoxicity in male Wistar rat. Journal of Food Biochemistry, 45(3), e13341. DOI: 10.1111/jfbc.13341
Akinyemi, A. J., Onyebueke, N., Faboya, O. A., Onikanni, S. A., Fadaka, A., & Olayide, I. (2017). Curcumin inhibits adenosine deaminase and arginase activities in cadmium-induced renal toxicity in rat kidneys. journal of food and drug analysis, 25(2), 438-446. https://doi.org/10.1016/j.jfda.2016.06.004
Longobardi, C., Damiano, S., Andretta, E., Prisco, F., Russo, V., Pagnini, F., … & Ciarcia, R. (2021). Curcumin Modulates Nitrosative Stress, Inflammation, and DNA Damage and Protects against Ochratoxin-A-Induced Hepatotoxicity and Nephrotoxicity in Rats. Antioxidants, 10(8), 1239. https://doi.org/10.3390/antiox10081239
Orr, S. E., & Bridges, C. C. (2017). Chronic Kidney Disease and Exposure to Nephrotoxic Metals. International journal of molecular sciences, 18(5), 1039. https://doi.org/10.3390/ijms18051039
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