Some Marker Enzymes and Histological Alteration on the Administration of Tramadol Hydrochloride on Rat Liver

Simeon, George Gborienemi; Abbey, Silas Tonye

doi:10.4236/mri.2018.71002

Cited by 3 publications

(2 citation statements)

References 16 publications

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“…Several experimental studies indicated that the Reactive Oxygen Species (ROS) production should be considered a TR-induced toxicity mechanism. Therefore, Oxidative Stress (OS) following TR exposure induces toxicity and damage in different organs [11][12][13][14][15]. OS is defined as overproduction and accumulation of free radicals, including ROS in cells and tissues, and the inability of the biological system to detoxify these reactive products.…”

Section: Introductionmentioning

confidence: 99%

Tramadol-Induced Organ Toxicity via Oxidative Stress : A Review Study

Mohammadnejad

Soltaninejad

2022

IJMTFM

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Background: Tramadol (TR) is a synthetic opioid-like centrally acting analgesic used for moderate to severe pain management in various diseases. Numerous investigations have supported the association between tramadol use and increased levels of oxygen-free radicals. Mass production of reactive oxygen species produces secondary toxic compounds. This could damage the internal components of the cell and ultimately causes organ damage. There exists a growing trend of tramadol abuse and the increasing reports of poisoning, abuse, and mortality due to this drug. Thus, the present study aimed to review the animals and human studies on the effects of acute and chronic exposure of tramadol in inducing organ toxicities through oxidative stress. Methods: Pubmed, Google Scholar, and Scopus bibliographic databases were searched for studies that investigated oxidative stress as a mechanism of toxicity by tramadol. A manual search of reference lists of the retrieved articles was conducted. Data were collected from 2000 to 2021 (up to June 2021). Results: From 28 articles concerning experimental and human studies of TR-induced oxidative stress organ damage, which included in this review, the occurrence of lipid peroxidation, alteration in the levels of total antioxidant capacity, and other oxidative stress biomarkers in many organs such as the brain, liver, kidney, adrenal and lung in the experimental studies of tramadol exposure have been observed. Conclusion: Oxidative stress could be considered the most critical toxic mechanism in TR-induced tissue damage.

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Section: Introductionmentioning

confidence: 99%

Tramadol-Induced Organ Toxicity via Oxidative Stress : A Review Study

Mohammadnejad

Soltaninejad

2022

IJMTFM

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“…Tramadol is a centrally acting analgesic drug, used for management of moderate to severe pain in a variety of diseases as osteoarthritis, fibromyalgia, diabetic neuropathy, neuropathic pain, and even perioperative pain in human patients (El-Gaafarawi, 2006); in addition, it is used in the treatment of opiate withdrawal and premature ejaculation (Simeon & Abbey, 2018). Its analgesic effect is due to its partial affinity for the mu-opiate receptor as well as its inhibition of the reuptake of norepinephrine and serotonin (Shadnia et al, 2008).…”

Section: Introductionmentioning

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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