Role of homocysteine metabolism in animal reproduction: A review

Rizzo, Annalisa; Sciorsci, Raffaele Luigi

doi:10.1016/j.rvsc.2018.11.011

Cited by 12 publications

(6 citation statements)

References 83 publications

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“…In line with our findings, the involvement of HCY in the induction of mitochondrial dysfunction in rat ischemic brain [31] and reproduction disorders including reduced fertility, suppressed fertilization, and the developmental competence of oocytes and embryos, increased risk of recurrent miscarriage, placental infarction, and congenital defects was reported [27,29,30]. In addition, the protective role of melatonin against HCY-induced oxidative injury, through decreasing the levels of Caspase-3 and BAX and increasing BCL2, has been observed in human umbilical vein endothelial cells (HUVECs) and hippocampus of rats [51,52].…”

Section: Oxidative Medicine and Cellular Longevitysupporting

confidence: 90%

“…The universal methyl donor Sadenosylmethionine (SAMe) level is expected to be consumed by NAM to produce metNAM and S-adenosylhomocysteine (SAH), which is converted to HCY by the activity of AHCY, also known as SAH hydrolase [15,17,26]. Hyperhomocysteinemia (HHCY), an elevated level of HCY, is a cytotoxic condition involved in cardiovascular disorders, Alzheimer, Parkinson's, inflammations, and heart diseases [27,28]. Also, HHCY is associated with reduced fertility, risk of recurrent miscarriage and placental infarction, pregnancy loss at early stages, and premature birth with high incidence of congenital defects [27,29].…”

Section: Introductionmentioning

confidence: 99%

“…Hyperhomocysteinemia (HHCY), an elevated level of HCY, is a cytotoxic condition involved in cardiovascular disorders, Alzheimer, Parkinson's, inflammations, and heart diseases [27,28]. Also, HHCY is associated with reduced fertility, risk of recurrent miscarriage and placental infarction, pregnancy loss at early stages, and premature birth with high incidence of congenital defects [27,29]. Additionally, elevated levels of follicular HCY were associated with the poor qualities of oocytes and embryos in polycystic ovary syndrome patients undergoing assisted reproduction [30].…”

Section: Introductionmentioning

confidence: 99%

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Melatonin Alleviates the Toxicity of High Nicotinamide Concentrations in Oocytes: Potential Interaction with Nicotinamide Methylation Signaling

Sheikh

Mesalam

Song

et al. 2021

Oxidative Medicine and Cellular Longevity

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Despite the numerous studies on melatonin and nicotinamide (NAM, the active form of vitamin B3), the linkage between these two biomolecules in the context of signaling pathways regulating preimplantation embryo development has not yet been investigated. In this study, we used bovine oocyte model to elucidate the effect of melatonin on the developmental competence of oocytes under the stress of high NAM concentrations. Results showed that NAM (20 mM) administration during in vitro maturation (IVM) significantly reduced oocyte maturation and actin distribution, while induced reactive oxygen species (ROS) accumulation and mitochondrial dysfunction, the multiple deleterious effects that were alleviated by melatonin (10−7 M). The RT-qPCR and/or immunofluorescence showed upregulation of the apoptosis (Caspase-3, Caspase-9, and BAX), autophagy (Beclin-1, LC3A, LC3B, ATG7, LAMP1, and LAMP2), cell cycle (P21, P27, and P53), and DNA damage (COX2 and 8-OxoG) specific markers in oocytes matured under NAM treatment, compared to NAM-melatonin dual-treated and the untreated ones. In addition, the total cleavage and blastocyst development rate, as well as the total number of cells and the inner cell mass (ICM) per blastocyst, were reduced, while DNA fragmentation was induced, in the group of NAM sole treatment than NAM-melatonin cotreatment and control. Inspecting the underlying mechanisms behind NAM-associated toxicity revealed an increase in transcription pattern of NAM methylation (NNMT and AHCY) genes in NAM-treated oocytes while the opposite profile was observed upon melatonin supplementation. In conclusion, to our knowledge, this is the first study reporting that melatonin can protect oocytes and embryos from NAM-induced injury through its ROS-scavenging activity together with potential interaction with NAM methylation signaling.

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Section: Oxidative Medicine and Cellular Longevitysupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Melatonin Alleviates the Toxicity of High Nicotinamide Concentrations in Oocytes: Potential Interaction with Nicotinamide Methylation Signaling

Sheikh

Mesalam

Song

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Homocysteine (Hcy) is metabolized in kidneys and liver, whereas in the pancreas and small intestine transsulfuration takes place. In the human body after the production of the low level of Hcy, almost 3% circulate freely in the body, with the majority of Hcy present in bound form with other molecules or in disulfide form (Rizzo & Sciorsci, 2018). Total plasma homocysteine (tHcy) is the sum of the circulating Hcy molecules either in its reduced or oxidized forms.…”

Section: Introductionmentioning

confidence: 99%

Cysteine and homocysteine as biomarker of various diseases

Rehman

Shabbir

Inam‐Ur‐Raheem

et al. 2020

Food Science & Nutrition

187

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Cysteine and homocysteine (Hcy), both sulfur‐containing amino acids (AAs), produced from methionine another sulfur‐containing amino acid, which is converted to Hcy and further converted to cysteine. This article aims to highlight the link between cysteine and Hcy, and their mechanisms, important functions, play in the body and their role as a biomarker for various types of diseases. So that using cysteine and Hcy as a biomarker, we can prevent and diagnose many diseases. This review concluded that hyperhomocysteinemia (elevated levels of homocysteine) is considered as toxic for cells and is associated with different health problems. Hyperhomocysteinemia and low levels of cysteine associated with various diseases like cardiovascular diseases (CVD), ischemic stroke, neurological disorders, diabetes, cancer like lung and colorectal cancer, renal dysfunction‐linked conditions, and vitiligo.

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“…3 Normal concentrations of human plasma Hcy in healthy adults have been reported to the extent of 5–10 μM. 4 The main metabolic pathways of Hcy are remethylation and transsulfuration. 5 Related studies have shown that the imbalance between Hcy production and metabolism leads to excessive increases of Hcy in plasma and urine, and high levels of Hcy can cause hyperhomocysteinemia (HHcy).…”

Section: Introductionmentioning

confidence: 99%