Acetylated Oligopeptide and N-acetyl cysteine Protected Against Oxidative Stress, Inflammation, Testicular-Blood Barrier Damage, and Testicular Cell Death in Iron-Overload Rat Model

Ezzat, Ghada M; Nassar, Ahmed; Bakr, Marwa H.; Mohamed, Shimma; Nassar, Gamal A. Y.; Kamel, Amira A.

doi:10.1007/s12010-023-04457-2

Cited by 8 publications

(2 citation statements)

References 57 publications

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“…Combined administration of LA plus NAC significantly exhibited a better histological result against CIS testicular toxicity. Recent studies 19,103 have confirmed the testicular protective effect of both LA and NAC against toxic agents.…”

Section: Discussionmentioning

confidence: 86%

Mitigative Effects of l-Arginine and N-Acetyl Cysteine against Cisplatin-Induced Testicular Dysfunction and Toxicity through the Regulation of Antioxidant, Anti-inflammatory, and Antiapoptotic Markers: Role of miR-155 and miR-34c Expression

Gad,

Abdelghaffar Emam,

Eldeeb

et al. 2024

ACS Omega

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Section: Discussionmentioning

confidence: 86%

Mitigative Effects of l-Arginine and N-Acetyl Cysteine against Cisplatin-Induced Testicular Dysfunction and Toxicity through the Regulation of Antioxidant, Anti-inflammatory, and Antiapoptotic Markers: Role of miR-155 and miR-34c Expression

Gad,

Abdelghaffar Emam,

Eldeeb

et al. 2024

ACS Omega

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“…NAC attenuates the blood-testis barrier damage caused by the SR X-ray [128] and may be used as a preventive measure against iron overload-induced testicular damage [129]. The antioxidant effect of NAC reduces the damage caused by various chemicals and radiation to testicular cells [130][131][132][133].…”

Section: Testosterone and Vitamin D Metabolismmentioning

confidence: 99%

The Impact of Vitamin D and L-Cysteine Co-Supplementation on Upregulating Glutathione and Vitamin D-Metabolizing Genes and in the Treatment of Circulating 25-Hydroxy Vitamin D Deficiency

Jain,

Justin Margret,

Abrams

et al. 2024

Nutrients

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Vitamin D receptors are expressed in many organs and tissues, which suggests that vitamin D (VD) affects physiological functions beyond its role in maintaining bone health. Deficiency or inadequacy of 25(OH)VD is widespread globally. Population studies demonstrate that a positive association exists between a high incidence of VD deficiency and a high incidence of chronic diseases, including dementia, diabetes, and heart disease. However, many subjects have difficulty achieving the required circulating levels of 25(OH)VD even after high-dose VD supplementation, and randomized controlled clinical trials have reported limited therapeutic success post-VD supplementation. Thus, there is a discordance between the benefits of VD supplementation and the prevention of chronic diseases in those with VD deficiency. Why this dissociation exists is currently under debate and is of significant public interest. This review discusses the downregulation of VD-metabolizing genes needed to convert consumed VD into 25(OH)VD to enable its metabolic action exhibited by subjects with metabolic syndrome, obesity, and other chronic diseases. Research findings indicate a positive correlation between the levels of 25(OH)VD and glutathione (GSH) in both healthy and diabetic individuals. Cell culture and animal experiments reveal a novel mechanism through which the status of GSH can positively impact the expression of VD metabolism genes. This review highlights that for better success, VD deficiency needs to be corrected at multiple levels: (i) VD supplements and/or VD-rich foods need to be consumed to provide adequate VD, and (ii) the body needs to be able to upregulate VD-metabolizing genes to convert VD into 25(OH)VD and then to 1,25(OH)2VD to enhance its metabolic action. This review outlines the association between 25(OH)VD deficiency/inadequacy and decreased GSH levels, highlighting the positive impact of combined VD+LC supplementation on upregulating GSH, VD-metabolizing genes, and VDR. These effects have the potential to enhance 25(OH)VD levels and its therapeutic efficacy.

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High Concentration of Iron Ions Contributes to Ferroptosis-Mediated Testis Injury

Liu,

Wang,

Xia

et al. 2024

Biol Trace Elem Res

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In order to explore the effect of different concentrations of iron ions on ferroptosis in mouse testes, Kunming mice were randomly divided into control group (normal saline), low iron concentration group (25mg/kg), high iron concentration group (70mg/kg) and deferoxamine group (40mg/kg). The mice were injected continuously for 7 days and their body weight was measured. At the end of the experiment, the organ weight, sperm count, and malformation rate were measured. Testicular tissue, the pathological and ultrastructural changes in spermatogenic tubules were also observed by using hematoxylin eosin (HE) staining and transmission electron microscopy. The changes in transcription levels of related genes and serum biochemical indicators were measured in mouse testicular tissues. The results showed that higher iron concentration may inhibit the growth of mice, reduce the organ coe cients of testis, heart, and liver, and increase the rate of sperm malformation and mortality. Supplementation of iron ion in high concentration can negatively affect the male reproductive system by reducing the sperm count and causing malformation and structural damage in seminiferous tubules and sperm cells. In addition, the iron concentration also affected the immune response and blood coagulation ability by in uencing the red blood cells, white blood cells and platelets. The results showed that iron ions may affect mice testicular tissue and induce ferroptosis by altering the expression of ferroptosis related genes. Though, the degree of effect was different for the different concentrations of iron ions. The study also revealed the potential role of deferoxamine to inhibit the occurrence of ferroptosis. Though, the damages caused to the testis by deferoxamine supplementation suggests the need for further researches in this direction.

show abstract

Acetylated Oligopeptide and N-acetyl cysteine Protected Against Oxidative Stress, Inflammation, Testicular-Blood Barrier Damage, and Testicular Cell Death in Iron-Overload Rat Model

Cited by 8 publications

References 57 publications

Mitigative Effects of l-Arginine and N-Acetyl Cysteine against Cisplatin-Induced Testicular Dysfunction and Toxicity through the Regulation of Antioxidant, Anti-inflammatory, and Antiapoptotic Markers: Role of miR-155 and miR-34c Expression

Mitigative Effects of l-Arginine and N-Acetyl Cysteine against Cisplatin-Induced Testicular Dysfunction and Toxicity through the Regulation of Antioxidant, Anti-inflammatory, and Antiapoptotic Markers: Role of miR-155 and miR-34c Expression

The Impact of Vitamin D and L-Cysteine Co-Supplementation on Upregulating Glutathione and Vitamin D-Metabolizing Genes and in the Treatment of Circulating 25-Hydroxy Vitamin D Deficiency

High Concentration of Iron Ions Contributes to Ferroptosis-Mediated Testis Injury

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