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Attenuation of DOX-Associated Biochemical and Histological Brain Alterations
Ehab Y Abdelhiee1, Sabreen E Fadl2, Faten Elsayed3
1Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Matrouh University, Marsa Matruh, Egypt.
Background:
Doxorubicin (DOX) is a common anticancer drug used to treat various types of neoplasms. However, its use is associated with neurotoxic effects, including neuronal degeneration and damage.
Objective:
The principal objective of the current experiment was to examine the mechanisms underlying biochemical and histological brain alterations induced by DOX under acute experimental conditions. Moreover, the ameliorative effects of allicin (AC) and/or L-carnitine (LC) against DOX-induced biochemical and histological brain alterations were evaluated.
Methods:
A total of seven groups of Wistar rats (n = 49; male, 150 ± 50 g; 30 weeks old) were established, including the control, AC, LC, DOX, AC+DOX, LC+DOX and AC+LC+DOX groups. Biochemical analyses, oxidative stress and proinflammatory cytokines were assessed spectrophotometrically using ELISA, and the histomorphology of brain sections (cerebrum, cerebellum and hypothalamus) was evaluated.
Results:
Results revealed that treatment with DOX increased acetylcholinesterase (AChE) activity (p < 0.0001) with increased levels of malondialdehyde (MDA) and nitric oxide (NO) contents. Meanwhile, non-enzymatic (glutathione, GSH) levels and enzymatic (superoxide dismutase, SOD; catalase, CAT) antioxidant activities were decreased. In addition, acute experimental DOX conditions increased levels of proinflammatory cytokines and interleukins (ILs): IL-6 and IL-1β. Histopathologically, the brain sections showed neuronal degeneration and vacuolization. However, biochemical, oxidative, inflammatory and histological brain alterations caused by acute experimental DOX conditions were improved by AC and/or LC supplementation.
Conclusion:
In summary, our research showed that AC and/or LC attenuated acute DOX-associated biochemical, oxidative, inflammatory and histological brain alterations.
Insights
Doxorubicin (DOX) causes brain damage by increasing oxidative stress and inflammation. Allicin (AC) and L-carnitine (LC) effectively protected against these DOX-induced neurotoxic effects.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Doxorubicin (DOX) is a widely used chemotherapy agent.
- DOX treatment can lead to significant neurotoxic effects, including neuronal damage.
- Understanding the mechanisms of DOX-induced neurotoxicity is crucial for developing protective strategies.
Purpose of the Study:
- To investigate the biochemical and histological brain changes caused by acute Doxorubicin exposure.
- To evaluate the protective effects of allicin (AC) and L-carnitine (LC) against Doxorubicin-induced neurotoxicity.
Main Methods:
- Wistar rats were divided into seven groups, including control and treatment groups (AC, LC, DOX, AC+DOX, LC+DOX, AC+LC+DOX).
- Biochemical markers, oxidative stress indicators (MDA, NO, GSH), antioxidant enzyme activities (SOD, CAT), and proinflammatory cytokines (IL-6, IL-1β) were measured.
- Histopathological examination of brain tissues (cerebrum, cerebellum, hypothalamus) was performed.
Main Results:
- Doxorubicin treatment significantly increased acetylcholinesterase activity, MDA, and NO levels.
- DOX administration decreased non-enzymatic (GSH) and enzymatic (SOD, CAT) antioxidant levels.
- DOX elevated proinflammatory cytokines (IL-6, IL-1β) and caused neuronal degeneration and vacuolization in brain tissues.
- Allicin and/or L-carnitine supplementation ameliorated these biochemical, oxidative, inflammatory, and histological brain alterations induced by DOX.
Conclusions:
- Acute Doxorubicin exposure induces significant biochemical, oxidative, inflammatory, and histological brain damage.
- Allicin and L-carnitine demonstrate protective effects against Doxorubicin-induced neurotoxicity.
- AC and/or LC can be considered as potential adjunct therapies to mitigate Doxorubicin's side effects.
