Upregulation of Uric Acid Production and Caspase 3 Signalling Mediates Rohypnol-Induced Cardiorenal Damage

Akhigbe, R.E.; Oladipo, AT; Oyedokun, P A; Hamed, Moses Agbomhere; Okeleji, L O; Ajayi, Ayodeji Folorunsho

doi:10.1007/s12012-022-09723-z

Cited by 7 publications

(5 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, it is important to note that UA may act as an antioxidant ( 45 ) and can curtail radical-forming systems ( 46 ). The pro-oxidant activity of UA can result from its reaction with other oxidants to produce radicals that majorly disrupt cellular activities ( 47 ). The lipophilic environment created due to the accumulation of lipids, in turn, creates an unfavourable environment for the antioxidant activity of UA ( 46 ), and the uric acid is thereby converted to oxidants by the oxidised lipids ( 49 ).…”

Section: Discussionmentioning

confidence: 99%

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

Odetayo

Adeyemi

Olayaki

2023

Front. Reprod. Health

View full text Add to dashboard Cite

IntroductionBisphenol F (BPF), an alternative to bisphenol A has been implicated as a gonadotoxic substance. BPF has been shown to induce hormonal imbalance and testicular oxidative damage. However, the mechanism associated with BPF-induced testicular toxicity has not been fully explored. This study was designed to explore the role of tumor protein (p53)/ B-cell lymphoma 2 (BCl-2) signaling and oestrogen receptor beta (Erβ) in BPF-induced testicular toxicity.MethodsMale Wistar rats were randomized into control (Cntrl), BPF-treated (10, 30, and 50 mg/kg for low dose (BPF-L), medium dose (BPF-M), and high dose (BPF-H) respectively), and BPF-treated recovery (Cntrl-R, BPF-L-R, BPF-M-R, and BPF-H-R). The administration was via gavage and lasted for 28 days and the animals in the recovery groups were allowed 28-days exposure free period for recovery from BPF exposure.ResultsBPF resulted in the distortion of the testicular histoarchitecture, which was accompanied by a significant rise in testicular gamma-lutamyl transferase and lactate dehydrogenase activities but a decline in sorbitol dehydrogenase activities. Also, BPF caused a significant reduction in plasma gonadotropin-releasing hormone, luteinising hormone, follicle-stimulating hormone, and testosterone, which was associated with the downregulation of testicular 3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase activities. Furthermore, BPF induced testicular inflammation, redox imbalance, and apoptosis, accompanied by distortion in p53/BCl-2 signaling and overexpression of Erβ. Again, the observed toxic effects of BPF were dose-dependent and not completely reversed by BPF cessation.DiscussionBisphenol F induced gonadotoxicity by distorting p53/BCl2 signaling and the expression of Erβ. These observed alterations were not completely reversed after the cessation of BPF exposure.

show abstract

Section: Discussionmentioning

confidence: 99%

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

Odetayo

Adeyemi

Olayaki

2023

Front. Reprod. Health

View full text Add to dashboard Cite

show abstract

“…Although UA exerts antioxidant activity by chelating metal ions such as iron and copper and converting them to their poorly active forms [ 34 ], it forms free radicals when it interacts with peroxynitrite [ 35 , 36 ], and oxidized lipids [ 37 ]. Studies have reported compelling evidence that implicate UA as a trigger of oxidative stress, inflammation, and apoptosis [ 38–40 ]. Our findings in this study indicate that IR-induced increased MDA and reduced GSH may have resulted from I/R – led elevated XO activity and UA levels.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin-mediated downregulation of VCAM-1 and XO/UA/caspase 3 signaling averts oxidative damage and apoptosis induced by ovarian ischaemia/reperfusion injury

Afolabi

Hamed²,

Anyogu

et al. 2022

Redox Report

Self Cite

View full text Add to dashboard Cite

Background Oxidative damage is critical in the pathogenesis of ovarian ischaemia/reperfusion (I/R) injury, and statins have been reported to exert antioxidant activity. However, the role of VCAM-1 and xanthine oxidase (XO)/uric acid (UA) in ovarian I/R injury is not known. Also, whether or not atorvastatin exerts antioxidant activity like other statins is unclear. Objectives This study investigated the involvement of VCAM-1 and XO/UA in ovarian I/R injury and the likely protective role of atorvastatin. Methods Forty female Wistar rats were randomized into sham-operated, ischaemia, ischaemia/reperfusion (I/R), ischaemia and atorvastatin, and I/R and atorvastatin. Results In comparison with the sham-operated group, atorvastatin blunted ischaemia and I/R-induced distortion of ovarian histoarchitecture and follicular degeneration. Also, atorvastatin alleviated ischaemia and I/R-induced rise in XO, UA, and malondialdehyde, which was accompanied by inhibition of ischaemia and I/R-induced reductions in reduced glutathione level, enzymatic antioxidant activities and increase in myeloperoxidase activity and TNF-α and IL-6 levels by atorvastatin treatment. Additionally, atorvastatin blocked ischaemia and I/R-induced increase in VCAM-1 expression, caspase 3 activity, 8-hydroxydeoxyguanosine level and ovarian DNA fragmentation index. Conclusion For the first time, this study revealed that atorvastatin-mediated downregulation of VCAM-1 and XO/UA/caspase 3 signaling averts oxidative injury, inflammation, and apoptosis induced by ovarian ischaemia/reperfusion injury.

show abstract

“…The body and renal weights of the animals were recorded using electronic weighing scale (Lisay, China). The renal organo-somatic index (OSI) was determined as renal weight/body weight X 100% ( 38 ).…”

Section: Methodsmentioning

confidence: 99%

“…Histopathological evaluation was performed as previously reported ( 3 , 38 ). The renal tissues were transversely cut in slabs of about 0.5 cm thick and fixed in Bouin’s fluid for 24 h and then transferred to 70% alcohol for dehydration.…”

Section: Methodsmentioning

confidence: 99%

Moringa oleifera-based feed supplement protects against renal ischaemia/reperfusion injury via downregulation of Bax/caspase 3 signaling

Afolabi,

Akhigbe,

Hammed

et al. 2024

Front. Nutr.

View full text Add to dashboard Cite

IntroductionIschaemia/reperfusion (I/R) may lead to acute kidney injury via the induction of oxidative stress. On the other hand, Moringa oleifera has been reported to exert antioxidant activities. This study was designed to assess whether or not Moringa oleifera-based feed supplement could prevent I/R-induced renal injury.Materials and methodsRenal I/R was induced by occluding the right renal artery for 30 min followed by a 2-h reperfusion.ResultsRenal I/R led to increased absolute renal weight and renal organo-somatic weight index. Renal I/R also caused distortion of renal histoarchitecture and impaired renal function evidenced by elevated serum creatinine and blood urea nitrogen. In addition, renal I/R significantly elevated renal levels of hydrogen peroxide, MDA, and advanced oxidation protein products, but suppressed the levels of reduced glutathione, protein thiol, and non-protein thiol, and the activities of superoxide dismutase and glutathione peroxidase. In addition, renal I/R up-regulated myeloperoxidase activity and the renal levels of NO, TNF-α, and IL-6. Renal I/R also up-regulated Bax and caspase 3 expression in the kidney. Furthermore, I/R-driven structural and biochemical alterations were markedly inhibited by Moringa oleifera-based feed supplement.DiscussionThese results suggest that Moringa oleifera-based feed supplement may preserve the gross and histoarchitectural integrity of the kidney as well as renal function via downregulation of Bax/caspase 3 signaling by targeting oxidative stress, inflammation and apoptosis in the kidney of I/R rat.

show abstract

Upregulation of Uric Acid Production and Caspase 3 Signalling Mediates Rohypnol-Induced Cardiorenal Damage

Cited by 7 publications

References 67 publications

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

Atorvastatin-mediated downregulation of VCAM-1 and XO/UA/caspase 3 signaling averts oxidative damage and apoptosis induced by ovarian ischaemia/reperfusion injury

Moringa oleifera-based feed supplement protects against renal ischaemia/reperfusion injury via downregulation of Bax/caspase 3 signaling

Contact Info

Product

Resources

About