Lycopene protects against renal cortical damage induced by nandrolone decanoate in adult male rats

Shalaby, Abdalla; Shaer, Dina Fouad El

doi:10.1016/j.aanat.2019.05.003

Cited by 11 publications

(6 citation statements)

References 41 publications

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“…Consistent with the present study, the researchers suggested that N consumption at doses of 10 mg/kg (9) and 20 mg/kg could decrease the activity of catalase, glutathione peroxidase and SOD in the cardiac and kidney tissues of rats. Increased renal hypertrophy in these studies was also reported to be associated with decreased clearance of creatinine, indicating renal dysfunction (13); however, inconsistent with the present study, eight weeks of N consumption at dose of 10 mg/kg/week had no significant effect on renal oxidative changes, although histopathological results showed that glomerular filtration was impaired and blood creatinine levels increased (14) Differences in baseline levels or toxicity inducing interventions of renal injury appear to be the reasons for the differences in the results of these two studies. The present study was performed only with N to evaluate its toxicity in the kidney tissue, but in Shalaby et al's study administration of 4 mg/kg/day was also performed.…”

Section: Discussioncontrasting

confidence: 94%

Effect of Nandrolone Treatment with and without Resistance Training on Superoxide Dismutase Concentration and Pathology of Kidney Tissue in Rats

Heidari

Hosseini

Azarbayjani

2020

J Clin Res Paramed Sci

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Background: The prevalence of anabolic steroids abuse in athletes and non-athletes is associated with the risk of injury to various organs, but there are limited studies of oxidative changes in kidney tissue following nandrolone (N) administration. Objectives: the aim of this study was to investigate the effect of N treatment with and without resistance training (RT) on superoxide dismutase (SOD) concentration and tissue pathology of kidney tissue in rats. Methods: In this experimental study, 20 male Wistar rats were randomly divided into four groups of five rats including 1) control (C), 2) sham (normal saline) (Sh), 3) N, and 4) N + RT. Groups 3 and 4 received 10 mg/kg N peritoneally, and the N + RT group performed 1 m ladder climbing for eight weeks and three sessions per week. SOD levels of kidney tissue were measured by ELISA and radioimmunoassay. Hematoxylin-eosin (H&E) staining was used to evaluate oxidative stress levels in kidney tissue. One-way ANOVA with Bonferroni’s post- hoc tests were used for analysis of research findings in SPSS version 22 (P ≤ 0.05). Results: SOD levels in the C group were higher than the Sh (P = 0.001), N (P = 0.001), and N + RT (P = 0.001) groups. SOD levels were lower in the Sh group than in the N (P = 0.049) and N + RT (P = 0.001) groups. However, there was no significant difference in SOD levels in the N + RT group and N group (P = 0.28). Also, oxidative stress levels were normal in tissue studies in all groups. Conclusions: It seems that Ntreatment with and without RT reduces SOD activity in kidney tissue, but more studies are needed in this regard given the normality of tissue oxidative stress results.

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Section: Discussioncontrasting

confidence: 94%

Effect of Nandrolone Treatment with and without Resistance Training on Superoxide Dismutase Concentration and Pathology of Kidney Tissue in Rats

Heidari

Hosseini

Azarbayjani

2020

J Clin Res Paramed Sci

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“…Some paraffin sections were stained using the avidin–biotin immunohistochemical technique for P53 and Bax . The immunohistochemistry was done according to Shalaby & El Shaer (2019).…”

Section: Methodsmentioning

confidence: 99%

Tramadol Promotes Oxidative Stress, Fibrosis, Apoptosis, Ultrastructural and Biochemical alterations in the Adrenal Cortex of Adult Male Rat with Possible Reversibility after Withdrawal

et al. 2020

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Tramadol is a centrally acting analgesic drug, used for the management of moderate to severe pain in a variety of diseases. The long-term use of tramadol can induce endocrinopathy. This study aimed to evaluate the effect of tramadol dependence on the adrenal cortex and the effect of its withdrawal. Thirty adult male rats were divided into three experimental groups: the control group, the tramadol-dependent group that received increasing therapeutic doses of tramadol orally for 1 month, and the recovery group that received tramadol in a dose and duration similar to the previous group followed by a withdrawal period for another month. Specimens from the adrenal cortex were processed for histological, immunohistochemical, enzyme assay, and quantitative real-time PCR (RT-qPCR) studies. Tramadol induced a significant increase in malondialdehyde level and a significant decrease in the levels of glutathione peroxidase and superoxide dismutase. A significant decrease in the levels of adrenocorticotrophic hormones, aldosterone, cortisol, corticosterone, and dehydroepiandrosterone sulfate was also detected. Severe histopathological changes in the adrenal cortex were demonstrated in the form of disturbed architecture, swollen cells, and shrunken cells with pyknotic nuclei. Inflammatory cellular infiltration and variable-sized homogenized areas were also detected. A significant increase in P53 and Bax immunoreaction was detected and confirmed by RT-qPCR. The ultrastructural examination showed irregular, shrunken adrenocorticocytes with dense nuclei. Dilated smooth endoplasmic reticulum, mitochondria with disrupted cristae, and numerous coalesced lipid droplets were also demonstrated. All these changes started to return to normal after the withdrawal of tramadol. Thus, it was confirmed that the long-term use of tramadol can induce severe adrenal changes with subsequent insufficiency.

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“…Magnanimous studies have demonstrated that LYC can alleviate renal toxicity. One study showed that LYC could mitigate histopathological changes such as vacuolation and renal tubular epithelial cell shedding . At the same time, LYC can also alleviate renal dysfunction caused by toxic substances such as methotrexate, etc.…”

Section: Introductionmentioning

confidence: 99%

“…One study showed that LYC could mitigate histopathological changes such as vacuolation and renal tubular epithelial cell shedding. 18 At the same time, LYC can also alleviate renal dysfunction caused by toxic substances such as methotrexate, 19 etc. However, few studies have been able to identify whether LYC may decrease DEHP-induced renal cell damage as well as the mechanism by which it does so.…”

Section: ■ Introductionmentioning

confidence: 99%

Lycopene Preventing DEHP-Induced Renal Cell Damage Is Targeted by Aryl Hydrocarbon Receptor

Li¹,

Zhao²,

Wang³

et al. 2021

J. Agric. Food Chem.

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Di (2-ethylhexyl) phthalate (DEHP) is an environmentally persistent and bioaccumulative plasticizer. Accumulation of DEHP in the body can eventually cause kidney damage. As a type of natural carotenoid, lycopene (LYC) has a potential protective effect on renal cells, but the protective mechanism has not yet been elucidated. The major goal of this study was to see how effective LYC was at treating DEHP-induced nephrotoxicity in mice. ICR mice were treated with DEHP (500 mg/kg BW/day or 1000 mg/kg BW/day) or LYC (5 mg/kg BW/day) for 28 days. Through histopathology and ultrastructure, we found that LYC attenuated DEHP-induced renal tubular cell and glomerular damage. LYC relieved DEHP-induced kidney injury evidenced by lower levels of blood urea nitrogen (Bun), creatinine (Cre), and uric acid (Uric). Meanwhile, the reduced expression of kidney injury molecule-1 (Kim-1) also supported it. Notably, LYC can alleviate the activity or content of cytochrome P450 system (CYP450s) interfered with by DEHP. In addition, LYC treatment reduced nuclear accumulation of DEHP-induced aromatic hydrocarbon receptor (AhR) and AhR nuclear transporter (Arnt), and its downstream target genes such as cytochrome P450-dependent monooxygenase (CYP) 1A1, 1A2, and 1B1 expression significantly decreased to normal in the LYC treatment group. In summary, LYC can mediate the AhR/Arnt signaling system to prevent kidney toxicity in mice caused by DEHP exposure.

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Lycopene protects against renal cortical damage induced by nandrolone decanoate in adult male rats

Cited by 11 publications

References 41 publications

Effect of Nandrolone Treatment with and without Resistance Training on Superoxide Dismutase Concentration and Pathology of Kidney Tissue in Rats

Effect of Nandrolone Treatment with and without Resistance Training on Superoxide Dismutase Concentration and Pathology of Kidney Tissue in Rats

Tramadol Promotes Oxidative Stress, Fibrosis, Apoptosis, Ultrastructural and Biochemical alterations in the Adrenal Cortex of Adult Male Rat with Possible Reversibility after Withdrawal

Lycopene Preventing DEHP-Induced Renal Cell Damage Is Targeted by Aryl Hydrocarbon Receptor

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