Co-administration of iron sulphate and nitroglycerin promoted oxidative stress and mild tissue damage in Wistar rats

Adeyemi, Oluyomi Stephen; Sulaiman, Faoziyat Adenike

doi:10.1007/s00580-013-1817-2

Cited by 7 publications

(8 citation statements)

References 17 publications

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“…The increased level of MPO and NO, consequent of arsenite intoxication may also have aided the lipid peroxidation as well as resultant oxidative cellular damage. Elevated production of NO can react with metals, reduced thiols, molecular oxygen and superoxide leading to adverse reactions (Bryan et al 2005;Gladwin et al 2005) leading to cellular damage (Adeyemi and Sulaiman 2014). Likewise, increased activity of MPO has been linked to oxidative cellular damage (Adeyemi and Akanji 2011b).…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats

Adeyemi

Meyakno²,

Akanji³

2017

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Study determined the influence of the inhibition of Kupffer cell functions by GdCl3 in arsenic intoxication. Twenty-four Wistar rats weighing between 150 and 160 g were randomly assigned into four groups. Group 1 received sodium arsenite (1.5 mg/kg b.w.) once a day, Group 2 received GdCl3 (2 mg/kg b.w.) once, 24 hours before commencing the arsenite (1.5 mg/kg b.w.) treatment. Group 3 received GdCl3 (2 mg/kg b.w.) once and subsequently given distilled water. Group 4 received distilled water only. The treatments were daily by oral gavage and lasted for 28 days. Animals were euthanized 24 hours after the last treatment. Arsenic exposure elevated the activities of rat plasma AST, ALT, ALP and γ-GT, indicative of liver injury. Arsenic exposure in rat lowered GSH concentration but potentiated inflammation and oxidative stress evidenced in the raised levels of MPO, NO and MDA. Rats with arsenic exposure were predisposed to atherosclerosis, lowering the HDL-C but elevated the LDL-C concentration. The histopathological assessment showed degenerating cellular lesion caused by arsenic. However, the inhibition of Kupffer cell functions by GdCl3 suppressed arsenic intoxication improving the liver function indices, oxidative stress status, lipid profile, neutrophilic inflammation and ultimately restored the cellular architecture. Data suggest that specific inhibition of Kupffer cells by GdCl3 protected against arsenic intoxication.

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Section: Discussionmentioning

confidence: 99%

“…The concentration of nitric oxide as nitrite/nitrate level was determined using the Greiss method according to method described by Ekanem et al (2009). The myeloperoxidase (MPO -EC 1.11.2.2) activity was determined as previously described (Adeyemi and Sulaiman 2014), according to the method by Eiserich et al (1998).…”

Section: Biochemical Assaysmentioning

confidence: 99%

Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats

Adeyemi

Meyakno²,

Akanji³

2017

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“…The enzymes measured have been implicated for the evaluation of liver injury arising from exposure to chemical compounds including drugs amongst others (Adeyemi and Akanji 2011b;Adeyemi and Sulaiman 2014). The decrease in the activities of AST and ALP in rat serum, heart, kidney, and liver following exposure to Pt nanoparticles may be due to inactivation of the enzyme molecules by the nanoparticles or their metabolites.…”

Section: Discussionmentioning

confidence: 99%

Biochemical and morphological changes in rats exposed to platinum nanoparticles

et al. 2016

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This study evaluated the toxicity potential of platinum (Pt) nanoparticles in Wistar rats. Wistar rats weighing between 180 and 193 g were randomly assigned into four groups. Animals in group 1 served as the control and received distilled water. Those in groups 2, 3, and 4 were administered with 10, 50, and 100 mg/kg body weight of Pt nanoparticles, respectively. At the end of treatments, the rats were fasted for 24 h and sacrificed under mild anesthesia. The blood and vital organs were collected and used for the biochemical and histopathological examinations. Pt nanoparticles caused significant alterations to the rat organ weights relative to the control. Also, the Pt nanoparticles altered the rat level of lipid profile and significantly elevated the atherogenic index relative to the control. The total protein level was increased in the tissues while the albumin decreased following nanoparticle treatment. Also, the nanoparticles inconsistently altered the level of serum urea and creatinine while the serum bilirubin level was raised. The activities of aspartate transaminase and alkaline phosphatase were reduced by nanoparticle treatments. However, the level of alanine aminotransferase (ALT) was inconsistently altered in serum and tissues by nanoparticle treatment with a significant elevation in the liver. Furthermore, nanoparticle exposure in rats caused several morphological lesions including inflammation and cellular degeneration, all of which were conspicuously absent in the control group. We show evidence that Pt nanoparticles potentiated alteration of rat biochemical and morphological indices in manners reminiscent of early cellular injury.

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“…This may be an early symptom of ensuing toxic events caused by the nanoparticle exposure. Previous studies have associated changes to body weight with toxicity of drugs or chemicals (Orisakwe et al, 2004;Adeyemi and Sulaiman, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…The alanine and aspartate aminotransferases (ALT and AST) are 'markers' of liver damage and can thus be used to assess liver cytolysis (Adeyemi and Sulaiman, 2014;Sulaiman and Ekanem, 2009). The administration of Ag/Au nanoparticles decreased the activities of AST and ALT in rat serum, liver, kidney and heart relative to the control.…”

Section: Discussionmentioning

confidence: 99%

Oral Exposure to Silver/Gold Nanoparticles: Status of Rat Lipid Profile, Serum Metabolites and Tissue Morphology

Sulaiman¹,

Akanji²,

Oloyede³

et al. 2015

J. of Medical Sciences

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Study investigated the effect of oral administration of gold-silver nanoparticles on rat biochemical parameters and tissue morphology. Wistar rats weighing approximately 180±7 g were randomly assigned into four groups. Animals in the control group received distilled water once daily for 30 days while, those in the treatment groups were administered 10, 50 and 100 mg kgG 1 b.wt. gold-silver nanoparticles. The rats were sacrificed under slight anesthesia, 24 h after the last treatments. Blood and vital organs including the heart, kidney and liver were collected and prepared for biochemical and histopathological determinations. Exposure to Ag/Au nanoparticles altered the rat serum lipid profile; lowering the HDL-C while raising the atherogenic index. Exposure of Ag/Au nanoparticles in rats caused significant alteration to the levels of serum albumin, total protein, bilirubin, urea and creatinine. The activities of alanine transaminase, aspartate transaminase and alkaline phosphatase in rat serum and tissues were also significantly altered by Ag/Au nanoparticles exposure. The histopathological examination revealed inflammation and cellular degeneration caused by exposure to the Ag/Au nanoparticles. We show evidence that Ag/Au nanoparticles elevated atherogenic index, as well as caused biochemical and morphological alterations, reminiscent of cellular injury.

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Co-administration of iron sulphate and nitroglycerin promoted oxidative stress and mild tissue damage in Wistar rats

Cited by 7 publications

References 17 publications

Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats

Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats

Biochemical and morphological changes in rats exposed to platinum nanoparticles

Oral Exposure to Silver/Gold Nanoparticles: Status of Rat Lipid Profile, Serum Metabolites and Tissue Morphology

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