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Red beetroot extract mitigates chlorpyrifos-induced reprotoxicity associated with oxidative stress, inflammation, and
Gadah Albasher1, Tarfa Albrahim2, Nouf Alsultan3
1Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia. galbeshr@ksu.edu.sa.
Abstract:
The goal of our investigation is to evaluate the potential protective efficacy of red beetroot extract (RBR) against testicular toxicity produced by CPF in rats. CPF exposure decreased the weight of testis and the levels of luteinizing hormone, follicle stimulating hormone and testosterone. CPF impaired also the oxidative status in favor of pro-oxidant molecules in the testicular tissue. Additionally, CPF stimulated the production of pro-inflammatory cytokines and their gene expression. Concomitantly, an apoptotic cascade has been observed upon CPF intoxication. However, RBR administration protected the testis tissue through modulating the hormonal level, inhibiting the oxidative damage, inflammation and the apoptotic responses following CPF intoxication. The obtained data recommend the use of RBR to prevent CPF-induced testicular damage via antioxidant, anti-inflammatory, and anti-apoptotic pathways.
Insights
Red beetroot extract (RBR) protects against chlorpyrifos (CPF)-induced testicular toxicity in rats. RBR mitigates hormonal imbalance, oxidative stress, inflammation, and apoptosis, supporting its use for preventing testicular damage.
Area of Science:
- Toxicology
- Reproductive Biology
- Natural Product Chemistry
Background:
- Chlorpyrifos (CPF) is an organophosphate pesticide linked to reproductive toxicity.
- Testicular damage involves hormonal disruption, oxidative stress, inflammation, and apoptosis.
- Red beetroot extract (RBR) possesses antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To evaluate the protective effects of RBR against CPF-induced testicular toxicity in a rat model.
- To investigate the underlying mechanisms of RBR's protective action.
Main Methods:
- Rats were exposed to CPF, with some receiving RBR co-administration.
- Testicular weight, hormone levels (LH, FSH, testosterone), oxidative stress markers, inflammatory cytokine levels, and gene expression were assessed.
- Apoptosis markers were evaluated to assess cellular damage.
Main Results:
- CPF exposure significantly reduced testicular weight, LH, FSH, and testosterone levels.
- CPF intoxication led to increased oxidative stress, pro-inflammatory cytokine production, and apoptotic activity in testicular tissue.
- RBR administration counteracted CPF-induced testicular toxicity by restoring hormonal balance, reducing oxidative damage, and suppressing inflammation and apoptosis.
Conclusions:
- RBR demonstrates significant protective efficacy against CPF-induced testicular toxicity in rats.
- The protective mechanisms of RBR involve antioxidant, anti-inflammatory, and anti-apoptotic pathways.
- RBR is a potential therapeutic agent for preventing pesticide-induced reproductive harm.
