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Published on: September 23, 2015
Molecular and histological changes in cerebral cortex and lung tissues under the effect of tramadol treatment
Eatemad A Awadalla1, Alaa-Eldin Salah-Eldin2
1Department of Zoology, Faculty of Science, Aswan University, P.O. 81528, Aswan, Egypt.
Abstract:
Tramadol abuse is one of the most frequent health problems in Egypt and worldwide. In most cases, tramadol abused by men face a problem with premature ejaculation. Tramadol like other opioids induces a decrease in plasma antioxidant levels, which may reflect a failure of the antioxidant defense mechanism against oxidative damage. The present work aimed to study the possible deleterious effects of oral administration of tramadol on brain and lung tissues in rats. Twenty adult male albino rats were divided into two groups; a control administered with normal saline and tramadol-treated (40mg/kg b.w.) group for 20 successive days. At the end of experimental period, blood was collected and specimens from brains and lungs were taken for histopathological and molecular studies. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) activities were measured in serum of control and tramadol-treated groups. Brain and lung specimens were histopathological evaluated using light microscopy. The expression levels of apoptotic related genes; Bcl-2, Bax and Caspase-3 were study in brain and lung tissues using RT-PCR analysis. We recorded a significant increase MDA level, while antioxidant enzymes; GSH, SOD and CAT were significantly decreased after tramadol-treatment. The obtained results revealed that tramadol induced a remarkable histomorphological changes in rats' brains (cerebral cortex and hippocampus) and severe histopathological changes in rats' lung when compared to that of control. On molecular level, the expression of the pro-apoptotic Bax and Caspase-3 showed a significant increase whereas the anti-apoptotic Bcl-2 decreased markedly indicating that tramadol is harmful at cellular level and can induce apoptotic changes in brain tissues. Our data confirmed the risk of increased oxidative stress, neuronal and pulmonary damage due to tramadol abuse. Although tramadol is reported to be effective in pain management, its toxicity should be kept in mind.
Insights
Tramadol abuse causes oxidative stress and damage to brain and lung tissues in rats. This study highlights the cellular toxicity and apoptotic changes induced by tramadol, emphasizing its risks beyond pain management.
Area of Science:
- Pharmacology
- Toxicology
- Neuroscience
Background:
- Tramadol abuse is a global health issue, often linked to sexual dysfunction in men.
- Opioid use, including tramadol, can deplete plasma antioxidant levels, suggesting impaired antioxidant defense.
- Oxidative stress is implicated in various tissue damages.
Purpose of the Study:
- To investigate the harmful effects of oral tramadol administration on rat brain and lung tissues.
- To assess the impact of tramadol on oxidative stress markers and antioxidant enzyme activities.
- To examine the molecular mechanisms of tramadol-induced cellular damage, including apoptosis.
Main Methods:
- Oral administration of tramadol (40mg/kg) to adult male rats for 20 days.
- Measurement of oxidative stress markers (MDA) and antioxidant enzymes (GSH, SOD, CAT) in serum.
- Histopathological examination of brain (cerebral cortex, hippocampus) and lung tissues using light microscopy.
- Analysis of apoptotic gene expression (Bcl-2, Bax, Caspase-3) in tissues via RT-PCR.
Main Results:
- Tramadol treatment significantly increased MDA levels and decreased GSH, SOD, and CAT activities.
- Histopathological analysis revealed significant brain and lung tissue damage in tramadol-treated rats.
- Molecular studies showed increased expression of pro-apoptotic genes (Bax, Caspase-3) and decreased anti-apoptotic gene (Bcl-2) expression.
Conclusions:
- Tramadol abuse induces significant oxidative stress and damages brain and lung tissues in rats.
- Tramadol promotes apoptosis in brain tissues, indicating cellular-level toxicity.
- The findings confirm the neurotoxic and pulmonary risks associated with tramadol abuse, underscoring the need for caution.
