The Effect of Some Heavy Metals on Kidney Tissue and Function
DOI:
https://doi.org/10.61132/obat.v2i5.738Keywords:
Cadmium chloride , lead acetate, Creatinine , Urea, Uric acidAbstract
This research tested the effect of cadmium chloride and lead acetate on kidney function and their impact on kidney tissues. The study included (30) white rats that were randomly divided into (6) groups:- The control group takes plain water orally for 30 days, the group that was given CdCl2 (5 mg/kg) of body weight, the group that was given CdCl2 10 mg/kg of body weight, the group that was given lead acetate 50 mg/kg of body weight, the group that was given lead acetate 100 mg/kg of body and the group that was given cadmium chloride 5mg/kg with lead acetate 50 mg/kg body weight with drinking water for a month .The results shown in Table (1) indicated a significant increase (P < 0.05) in the levels of urea, creatinine, and uric acid in the serum of groups treated with CdCl2 at doses of 5 and 100 mg/kg, and the groups treated with lead acetate at doses of 50 and 100 mg/kg, as well as the group that received CdCl2 at a dose of 5 mg/kg along with lead acetate at a dose of 50 mg/kg, comparison with the healthy group .As for histological sections, the results showed the following section of the renal of the group treated with cadmium chloride 5 mg/kg shows atrophic renal glomerulus, necrosis of cells lining Bowman’s capsule , necrosis of cells lining the convoluted tubule and a large increase in the space between the glomerulus and the capsule. As for the group treated with high-dose cadmium chloride showing necrosis of cells lining the glomerulus and degeneration of cells lining the renal tubules Fragmentation of the glomerulus. As for the group treated with lead acetate at a dose of 50 mg/kg showing renal glomerulonephrosis, proximal and distal convoluted tubule necrosis, and periglomerular space in an almost normal manner. A section of the kidney of the group treated with with high-dose lead acetate, showing atrophy of some renal glomeruli and congestion of blood vessels and showing blood congestion within the kidney tissue, and decomposition of the cells lining the urinary tubules , Cross-section of the kidney of the group treated with cadmium chloride 5 mg/kg and lead acetate 50 mg/kg body weight Shows destruction of renal glomeruli and swelling of renal tubule cells and necrosis of the kidney tissue with the appearance of hemorrhage Comparison with the healthy group
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References
Abel,B. J.; Carswell, G. and Elton, R.(1983). Randomised trial of clomiphene citrate treatment and vitamin C for male infertility. British Journal of Urology. 54, 780-784.
Al-Hajj , Hamid Ahmed (1998), Acoustic Microscopic Preparations (Microscopic Technologies), Theoretical Foundations and Applications - First Edition, Jordanian Book Center, Amman - Jordan, pp. 121-140, 149-186 , 221-232 .
AL-Imarah.F.J. Mehdi,J.K.(2000). Levels of trace metals in blood samples from steel casting workers. Basrah-Chemistry Collage of Sience Basrah Uni.
Al-Rubaye, R. H. (2017). Effect of aqueous leaves extract of Coriandrum sativumon histological structure and liver function of male Albino mice. Ibn AL- Haitham Journal For Pure and Applied Science, 29(1).
Ankrah. N.A.; Kamiya, Y.; Appiah, O.R.(1996). Lead levels andrelated biochemical findings. occurring in Ghanaian subjectsoccupationally exposed to lead. East Afr Med J 73: 375-379.
Bautista, C. J., Arango, N., Consuelo, P., Mitre-Aguilar, I. B., Trujillo, J., & Ramírez, V. (2024). Mechanism of Cadmium-induced nephrotoxicity. Toxicology, 153726.
Brand M.D. (2020). Riding the tiger—Physiological and pathological effects of superoxide and hydrogen peroxide generated in the mitochondrial matrix. Crit. Rev. Biochem. Mol. Biol. ;55:592–661. doi: 10.1080/10409238.2020.1828258.
Cameron, J.S.and Greger, R.(1998). Renal function and testing offunction. (Davidson AM, Cameron JS, Grunfeld JP, Kerr DNS, Rits E, Winearl GC eds.) Oxford Textbook of Clinical Nephrology pp.36-39.
Carmona A. Roudeau S, Ortega R.(2021). Molecular mechanisms of environmental metal neurotoxicity: A focus on the interactions of metals with synapse structure and function. Toxics.: 9(9):198.
Cooper, W.C.; Wong, O.and Kheifets, L. (1985). Mortality among employees of lead pattery plants and lead producing plants,Scand.J. work Evnviron. Health, NO:331-345.
Goto, Y.; Mandai, M.; Nakayama, Y.; Yamazaki, S.; Nakayama, F.N.; Isobe, L.; Sato, T. and Nitta, H. (2020) .Association of prenatal maternal blood lead levels with birth outcomes in the Japan Environment and Children's Study (JECS.(
Haneef.S.S.; Swarup, S.K.; Dwivedi, S.; Dash,P.K.(1998). Effects of concurrent exposure to lead and cadmium on renal function in goats. Small Ruminant Research, 28: 257-261. 29.
Junior, J. E. G. P., Moraes, P. Z., Rodriguez, M. D., Simoes, M. R., Cibin, F., Pinton, S., ... & Wiggers, G. A. (2020). Cadmium exposure activates NADPH oxidase, renin–angiotensin system and cyclooxygenase 2 pathways in arteries, inducing hypertension and vascular damage. Toxicology letters, 333, 80-89.
Kim, K. S., Lim, H. J., Lim, J. S., Son, J. Y., Lee, J., Lee, B. M., ... & Kim, H. S. (2018). Curcumin ameliorates cadmium-induced nephrotoxicity in Sprague-Dawley rats. Food and Chemical Toxicology, 114, 34-40.
Lee, W.-K., Probst, S., Scharner, B., Deba, T., Dahdouh, F., & Thévenod, F. (2024). Distinct concentration-dependent oxidative stress profiles by cadmium in a rat kidney proximal tubule cell line. Archives of Toxicology, 1–17.
McBride, M.B.; Rigden, S.; Haycock,G.B. (1998). Presymptomatic detection of familial juvenile.
Merce, A. L. R. (2024). Contaminated Waters and Depleted Soils: Impact in Nutrition II Biochemical Detoxification Pathways. EC Nutrition, 19, 1–29.
Nasiadek, M., Stragierowicz, J., & Kilanowicz, A. (2022). An Assessment of Metallothionein–Cadmium Binding in Rat Uterus after Subchronic Exposure Using a Long–Term Observation Model. International Journal of Molecular Sciences, 23(23), 15154.
Osman, A. T., Sharkawi, S. M., Hassan, M. I., Abo-Youssef, A. M., & Hemeida, R. A. (2021). Empagliflozin and neohesperidin protect against methotrexate-induced renal toxicity via suppression of oxidative stress and inflammation in male rats. Food and Chemical Toxicology, 155, 112406.
Priya, K. K., Thilagam, H., Muthukumar, T., Gopalakrishnan, S., and Govarthanan, M. (2023). Impact of microfiber pollution on aquatic biota: A critical analysis of effects and preventive measures. Science of The Total Environment, 163984
Rennke, H. G., & Denker, B. M. (2020). Renal pathology: the essentials.
Saini, S., and Dhania, G. (2020). Cadmium as an environmental pollutant: ecotoxicological effects, health hazards, and bioremediation approaches for its detoxification from contaminated sites. Bioremediation of industrial waste for environmental safety: Volume II: biological agents and methods for industrial waste management, 357-387.
Satarug, S., Vesey, D. A., Gobe, G. C., & Phelps, K. R. (2023). Estimation of health risks associated with dietary cadmium exposure. Archives of Toxicology, 97(2), 329-358.
Sharma, R., & Tiwari, S. (2021). Renal gluconeogenesis in insulin resistance: A culprit for hyperglycemia in diabetes. World Journal of Diabetes, 12(5), 556.
Sotomayor, C. G., Groothof, D., Vodegel, J. J., Eisenga, M. F., Knobbe, T. J., IJmker, J., ... & Bakker, S. J. (2021). Plasma cadmium is associated with increased risk of long-term kidney graft failure. Kidney International, 99(5), 1213-1224.
Swarup.D.and Dwivedi, S.K (1992). Changes in blood and cerebrospinal fluid in experimental lead toxicity in goats. Indian Journal of Animal Science, 62: 928-931.
Tieraztl Wochenschr 105: 290-293. 30. Khalil, M.F.; Gonick,H.C.; Cohen, A. (1992). Experimental model of lead nephropathy, effect of removal from lead exposure and chelationtreatment with DMSA. Environ Res 58: 35-54.
Trewin A.J., Bahr L.L., Almast A., Berry B.J., Wei A.Y., Foster T.H., Wojtovich A.P. (2019). Mitochondrial reactive oxygen species generated at the complex-ii matrix or intermembrane space microdomain have distinct effects on redox signaling and stress sensitivity in caenorhabditis elegans. Antioxid. Redox Signal. ;31:594–607.
Wang, Z., do Carmo, J. M., da Silva, A. A., Fu, Y., & Hall, J. E. (2020). Mechanisms of synergistic interactions of diabetes and hypertension in chronic kidney disease: role of mitochondrial dysfunction and ER stress. Current hypertension reports, 22, 1-10.
Ware, K., Yildiz, V., Xiao, M., Medipally, A., Hemminger, J., Scarl, R., ... & Brodsky, S. V. (2021). Hypertension and the kidney: Reduced kidney mass is bad for both normotensive and hypertensive rats. American Journal of Hypertension, 34(11), 1196-1202.
Weeden, R., Haesep, D.and Vyver, V.(1986).Lead ropathy. Amer.J.Kidney Disease. 3:380-385 .
Yan, L. J., and Allen, D. C. (2021). Cadmium-induced kidney injury: Oxidative damage as a unifying mechanism. Biomolecules, 11(11), 1575.
Yasir, F.; Muhammad, M.H.; Shoaib, B.A.and.Muhammad, A.F. (2008). Lead intoxication: The extent of problem and its management. Department of Physiology, Army Medical College,
Yokoyama, K.; Araki, S.; Akabayashi, A.(2000). Alteration of glucosemetabolism in the spinal cord of experimental lead poisoning rats:microdetermination of glucose utilization rate and distributionvolume. Ind Health 38: 221-223.
Yuzbaşıoglu, Y., Hazar, M., Aydın Dilsiz, S., Yücel, C., Bulut, M., Cetinkaya, S., Erdem, O., & Basaran, N. (2024). Biomonitoring of Oxidative-Stress-Related Genotoxic Damage in Patients with End-Stage Renal Disease. Toxics, 12(1), 69.
Zhang, C., Wang, X., Du, J., Gu, Z., and Zhao, Y. (2021). Reactive oxygen species-regulating strategies based treatment. Advanced Science, 8(3), 2002797
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