Assessment of the cellular integrity and expression of melatonin receptor (MTNR1A) in the retina assaulted by ethanol and acetaminophen

Adekeye, Adeshina Oloruntoba; Fafure, Adedamola Adediran

doi:10.1177/09603271221149010

Cited by 1 publication

(1 citation statement)

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“…Downregulation of MTNR1A can result in decreased testosterone levels within the testes, impacting normal physiological function ( Gao et al, 2019 ). Moreover, drugs such as ethanol and acetaminophen have been shown to reduce the expression of MTNR1A ( Adekeye and Fafure, 2022 ), thereby diminishing the regulatory effect of melatonin on tissue and cell development. Interestingly, melatonin itself is involved in regulating the expression of MTNR1A and has been found to play a role in mitigating anti-infection and anti-oxidative stress damage by inhibiting the loss of MTNR1A in amyotrophic lateral sclerosis ( Zhang et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Melatonin alleviates oxidative stress damage in mouse testes induced by bisphenol A

Qi,

Yang,

et al. 2024

Front. Cell Dev. Biol.

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We investigated the effect of melatonin on bisphenol A (BPA)-induced oxidative stress damage in testicular tissue and Leydig cells. Mice were gavaged with 50 mg/kg BPA for 30 days, and concurrently, were injected with melatonin (10 mg/kg and 20 mg/kg). Leydig cells were treated with 10 μmol/L of BPA and melatonin. The morphology and organ index of the testis and epididymis were observed and calculated. The sperm viability and density were determined. The expressions of melatonin receptor 1A and luteinizing hormone receptor, and the levels of malonaldehyde, antioxidant enzymes, glutathione, steroid hormone synthases, aromatase, luteinizing hormone, testosterone, and estradiol were measured. TUNEL assay was utilized to detect testicular cell apoptosis. The administration of melatonin at 20 mg/kg significantly improved the testicular index and epididymis index in mice treated with BPA. Additionally, melatonin promoted the development of seminiferous tubules in the testes. Furthermore, the treatment with 20 mg/kg melatonin significantly increased sperm viability and sperm density in mice, while also promoting the expressions of melatonin receptor 1A and luteinizing hormone receptor in Leydig cells of BPA-treated mice. Significantly, melatonin reduced the level of malonaldehyde in testicular tissue and increased the expression of antioxidant enzymes (superoxide dismutase 1, superoxide dismutase 2, and catalase) as well as the content of glutathione. Moreover, melatonin also reduced the number of apoptotic Leydig cells and spermatogonia, aromatase expression, and estradiol level, while increasing the expression of steroid hormone synthases (steroidogenic acute regulatory protein, cytochrome P450 family 17a1, cytochrome P450 17α-hydroxylase/20-lyase, and, 17β-hydroxysteroid dehydrogenase) and the level of testosterone. Melatonin exhibited significant potential in alleviating testicular oxidative stress damage caused by BPA. These beneficial effects may be attributed to melatonin’s ability to enhance the antioxidant capacity of testicular tissue, promote testosterone synthesis, and reduce testicular cell apoptosis.

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Section: Discussionmentioning

confidence: 99%