Differential/combined effect of water contamination with cadmium and nickel on tissues of rats

Novelli, Ethel L. B.; Hernandes, Rodrigo T.; Filho, José Luiz V. B. Novelli; Barbosa, L.L

doi:10.1016/s0269-7491(98)00109-2

Cited by 23 publications

(14 citation statements)

References 27 publications

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“…Another study reported that inhibited LDH activities with low and high contaminant exposure is frequently observed in ecotoxicological studies and conforms to the hormetic curve described by Stebbing [54]. Histopathological examination of rat liver: Liver is the target organ of heavy metals toxicity and its cells spell out hepatic enzymes into blood, which are commonly used as biochemical indicator index of hepatocellular damage [57]. The liver samples of DWHM-treated rats showed the focal hepatocytes damage and degeneration (Fig.…”

Section: Resultssupporting

confidence: 70%

“…Further, nickel intoxication caused a significant increase in the activities of GOT, GPT and alkaline phosphatase, probably due to hepatocyte membrane damage resulting in increased release and leakage out of these enzymes from the liver cytosol into the blood stream, which gives an indication on the hepatotoxic effect of this metal. Several studies indicated that an association control exists between nickel toxicity and the increased oxidative stress of rats [57].…”

Section: Resultsmentioning

confidence: 99%

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Effect of Source of Silica on Properties of Fe2O3/SiO2 Nanocompsites and Their Application on Hepatic Injury in Rats as Adsorbents for Removal of Heavy Metal from Drinking Water

Reda¹,

Al-Ghannam²,

El-Rahman³

2018

Asian J. Chem.

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Section: Resultssupporting

confidence: 70%

Section: Resultsmentioning

confidence: 99%

Effect of Source of Silica on Properties of Fe2O3/SiO2 Nanocompsites and Their Application on Hepatic Injury in Rats as Adsorbents for Removal of Heavy Metal from Drinking Water

Reda¹,

Al-Ghannam²,

El-Rahman³

2018

Asian J. Chem.

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“…Nickel is also found to induce oxidative injury in erythrocytes following generation of reactive oxygen species (ROS) [38]. In addition, the low hemoglobin concentration in this study may be as a result of a decrease in the succinyl and glycine pools, as well as the key enzymes such as, ALAD (Aminolevulinic Acid Dehydratase) that are required in the hem biosynthesis [43].…”

Section: Discussionmentioning

confidence: 69%

“…Mathur et al [37] showed that nickel accumulates in the kidneys by inducing many lesions which the most common are hyperemia and parenchymal cell degeneration with necrotic foci. Furthermore, it was well documented that nickel mainly accumulates in kidney because these organ contain most of the metallothionein, a metal binding protein with high affinity for nickel [38].…”

Section: Discussionmentioning

confidence: 99%

Effect of Silymarin Extracted From Silybum Marianum on Nickel Hematotoxicity and Nephrotoxicity in Male Albino Wistar Rats

Bouhalit

Kechrid

Elfeki

2017

Int J Pharm Pharm Sci

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Objective: The objective of this study was to investigate the effect of silymarin extract from Silybum marianum against nickel-induced alterations in haematological indices, kidney dysfunction and renal antioxidant defence system. Methods:Male albino Wistar rats were divided into four groups seven each. Control, silymarin, nickel and nickel plus silymarin. Silymarin was administrated orally (100 mg/kg b. wt) and nickel as nickel sulfate (NiSO4 6H2 Results:The treatment with nickel led to a significant decrease in body weight with an increase in both absolute and relative kidney weights and a significant increase in renal markers, which confirmed by histopathological alteration. A microcytic anemia was also observed, which was manifested by a reduction of red blood cells count (RBC), hemoglobin (Hb) concentration, platelet counts (Plt), hematocrit and white blood cells counts (WBC). The level of lipid peroxidation was increased. Whereas, GSH concentration and enzymatic antioxidants SOD, GSH-Px and CAT activities were decreased. The co-treatment with methanolic extract of milk thistle attenuated the variation in the hematological and renal markers, decreasing renal lipid peroxidation (p<0.05) with a concomitant increasing reduced glutathione content (p<0.01) and restoring the antioxidant enzymes (SOD, CAT, GSH-Px) in kidney, as well as an improvement in histological changes compared to those previously noticed in nickel group. 0) was given intraperitoneally (20 mg/kg b. wt) at alternative days. The experiment continued for three consecutive weeks. Body weight was recorded regularly. After overnight fasting, animals were killed and serum creatinine, serum urea, serum uric acid, hematological parameters and renal antioxidant markers were determined. Conclusion:To conclude, these findings demonstrated that silymarin extract effectively improved heamatotoxicity and nephrotoxicity caused by nickel.

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“…The measurements of creatinine, urea, and uric acid are considered a tool in the clinical diagnosis of renal dysfunction following acute and chronic oxidative kidney injury (27,28). The increased level of Ni in the kidney that was observed after Ni treatment could be explained by high affinity of metallothionein, a metal binding protein for Ni (29). The adverse effects of Ni on kidney function are potentially related to oxidative stress and overproduction of free radicals that can cause oxidation of biomolecules that vitamin C may act as a chelating agent of nickel leading to a lower cellular uptake of nickel, protecting consequently against kidney oxidative injury.…”

Section: Kidney Histopathological Changesmentioning

confidence: 99%

Vitamin C pretreatment protects from nickel-induced acute nephrotoxicity in mice

Kadi

Dahdouh

2016

Archives of Industrial Hygiene and Toxicology

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Nickel is an abundant carcinogenic and nephrotoxic metal whose activity leads to renal impairment. Previous studies have shown a protective effect of simultaneous vitamin C administration on acute and chronic nickel toxicity. However, very little research relating to the effect of vitamin C pretreatment in preventing nickel-induced acute nephrotoxicity is available. Therefore, the present study aimed to determine the efficiency of vitamin C (VC) pretreatment in preventing acute renal toxicity of nickel. Mice were pretreated orally with vitamin C (16.6 mg kg -1 body weight, b.w.) for seven consecutive days, prior to intraperitoneal (i.p.) administration of nickel chloride at different doses (3, 5, and 10 mg Ni kg -1 b.w.) for an exposure period of 24 hours. Thereafter, animals were killed and kidney tissue and blood samples were taken for histological examination and biochemical marker analyses. Vitamin C pretreatment alone did not alter the levels of serum kidney markers (creatinine, urea, and uric acid). However, treatment with Ni alone showed a significant increase in the levels of serum creatinine, urea, and uric acid with marked necrotic epithelial cells and infiltration by inflammatory cells in kidney sections as compared to the control group. Pretreatment with vitamin C and treatment with Ni at all doses tested for 24 hours showed a significant decrease in the levels of serum creatinine, urea, and uric acid, as well as an improvement in histological changes compared to those previously seen in the group treated with Ni alone. It is concluded that vitamin C pretreatment effectively improved renal function and tissue damage caused by nickel.

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Differential/combined effect of water contamination with cadmium and nickel on tissues of rats

Cited by 23 publications

References 27 publications

Effect of Source of Silica on Properties of Fe2O3/SiO2 Nanocompsites and Their Application on Hepatic Injury in Rats as Adsorbents for Removal of Heavy Metal from Drinking Water

Effect of Source of Silica on Properties of Fe2O3/SiO2 Nanocompsites and Their Application on Hepatic Injury in Rats as Adsorbents for Removal of Heavy Metal from Drinking Water

Effect of Silymarin Extracted From Silybum Marianum on Nickel Hematotoxicity and Nephrotoxicity in Male Albino Wistar Rats

Vitamin C pretreatment protects from nickel-induced acute nephrotoxicity in mice

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