Augmented oxidative stress and reduced mitochondrial function in ageing goat testis

Majrashi, Mohammed; Fujihashi, Ayaka; Almaghrabi, Mohammed; Fadan, Maali; Fahoury, Eddie; Ramesh, Sindhu; Govindarajulu, Manoj; Beamon, Haley; Bradford, Chastity; Bolden-Tiller, Olga; Dhanasekaran, Muralikrishnan

doi:10.1002/vms3.296

Cited by 6 publications

(8 citation statements)

References 43 publications

(47 reference statements)

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“…On the other hand, Oxidative stress can also cause apoptosis of Leydig cells in the testis, decrease androgen synthesis and secretion, and affect the normal development of male reproductive organs. Majrashi et al reported that effective and potent antioxidants in the feed could significantly reduce oxidative stress and improve mitochondrial function in ageing goat testis (Majrashi et al, 2020). Rahil Jannatifar et al demonstrated that N‐acetyl‐cysteine could increase the level of testosterone while resisting oxidation (Jannatifar et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Cordycepin, a major bioactive component ofCordyceps militaris, ameliorates diabetes‐induced testicular damage through the Sirt1/Foxo3a pathway

Huang

Zhou

et al. 2021

Andrologia

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Diabetes‐induced male dysfunction is considered as a worldwide challenge, and testicular damage mainly caused by oxidative stress is its most common manifestation. Cordycepin, a natural antioxidant, has been used in the treatment of diabetic complications. However, the protective action and underlying mechanism of cordycepin on hyperglycaemia‐induced testicular damage are unclear. This study aimed to investigate the protective effects and molecular mechanisms of cordycepin against diabetes‐induced testicular damage. The type 2 diabetes model was established in C57BL/6 male mice via high‐fat diet for 4 weeks and injected intraperitoneally with 50 mg/kg/day streptozotocin for five consecutive days. Then mice were treated with cordycepin (10 and 20 mg/kg, respectively) for 8 weeks. At the end of experiment, biochemical indicators, microstructure of testicular tissue, sperm morphology, TUNEL staining and protein expressions were evaluated. In the present study, cordycepin alleviated the testicular damage, restored disruption of the blood‐testis barrier, and improved spermatogenic function via the antiapoptotic and antioxidant capacity. Mechanistically, cordycepin significantly enhanced SIRT1 expression and triggered the activity of Foxo3a, further to induce the expression of its downstream antioxidant enzymes, including Mn‐SOD and CAT. These findings indicated that cordycepin could improve hyperglycaemia‐induced testicular damage by regulating downstream antioxidant enzymes activity through the SIRT1/Foxo3a signalling pathway.

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Section: Discussionmentioning

confidence: 99%

Cordycepin, a major bioactive component ofCordyceps militaris, ameliorates diabetes‐induced testicular damage through the Sirt1/Foxo3a pathway

Huang

Zhou

et al. 2021

Andrologia

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“…ROS content was determined by detecting the conversion of nonfluorescent chloromethyl‐DCF‐DA (2′, 7‐dichlorofluorescindiacetate, DCF‐DA) to fluorescent DCF using an excitation wavelength of 492 nm and an emission wavelength of 527 nm. This was done using spectrofluorometry 23,25–28 …”

Section: Methodsmentioning

confidence: 99%

“…The colorimetric method using thiobarbituric acid was used to quantify the lipid peroxide content. The formed thiobarbituric acid reactive substances (TBARS) were measured using a plate reader at 532 nm 23,26,28 …”

Section: Methodsmentioning

confidence: 99%

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Evaluate the in vitro effect of anthracycline and alkylating cytophosphane chemotherapeutics on dopaminergic neurons

Desai,

Majrashi,

Pathak

et al. 2024

Cancer Reports

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BackgroundIatrogenesis is an inevitable global threat to healthcare that drastically increases morbidity and mortality. Cancer is a fatal pathological condition that affects people of different ages, sexes, and races around the world. In addition to the detrimental cancer pathology, one of the most common contraindications and challenges observed in cancer patients is severe adverse drug effects and hypersensitivity reactions induced by chemotherapy. Chemotherapy‐induced cognitive neurotoxicity is clinically referred to as Chemotherapy‐induced cognitive impairment (CICI), chemobrain, or chemofog. In addition to CICI, chemotherapy also causes neuropsychiatric issues, mental disorders, hyperarousal states, and movement disorders. A synergistic chemotherapy regimen of Doxorubicin (Anthracycline‐DOX) and Cyclophosphamide (Alkylating Cytophosphane‐CPS) is indicated for the management of various cancers (breast cancer, lymphoma, and leukemia). Nevertheless, there are limited research studies on Doxorubicin and Cyclophosphamide's pharmacodynamic and toxicological effects on dopaminergic neuronal function.AimThis study evaluated the dopaminergic neurotoxic effects of Doxorubicin and Cyclophosphamide.Methods and ResultsDoxorubicin and Cyclophosphamide were incubated with dopaminergic (N27) neurons. Neuronal viability was assessed using an MTT assay. The effect of Doxorubicin and Cyclophosphamide on various prooxidants, antioxidants, mitochondrial Complex‐I & IV activities, and BAX expression were evaluated by Spectroscopic, Fluorometric, and RT‐PCR methods, respectively. Prism‐V software (La Jolla, CA, USA) was used for statistical analysis. Chemotherapeutics dose‐dependently inhibited the proliferation of the dopaminergic neurons. The dopaminergic neurotoxic mechanism of Doxorubicin and Cyclophosphamide was attributed to a significant increase in prooxidants, a decrease in antioxidants, and augmented apoptosis without affecting mitochondrial function.ConclusionThis is one of the first reports that reveal Doxorubicin and Cyclophosphamide induce significant dopaminergic neurotoxicity. Thus, Chemotherapy‐induced adverse drug reaction issues substantially persist during and after treatment and sometimes never be completely resolved clinically. Consequently, failure to adopt adequate patient care measures for cancer patients treated with certain chemotherapeutics might substantially raise the incidence of numerous movement disorders.

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“…2 ′ ,7 ′ -dichlorofluorescein diacetate (DCF-DA) (DCF, Calbiochem, 287810, 0.5%) dye-based fluorometric assay was performed to study the effect on ROS in the control and βhydroxybutyric treated HT-22 neurons [20].…”

Section: Effect Of β-Hydroxybutyric Acid On Reactive Oxygen Species (...mentioning

confidence: 99%

𝜷-hydroxybutyric acid attenuates oxidative stress and improves markers of mitochondrial function in the HT-22 hippocampal cell line

Majrashi

Altukri

Ramesh

et al. 2021

Journal of Integrative Neuroscience

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Ketone bodies have been the topic of research for their possible therapeutic neurotropic effects in various neurological diseases such as Parkinson's disease, dementia, and seizures. However, continuing research on ketone bodies as a prophylactic agent for decreasing the risk for various neurodegenerative diseases is currently required. In this paper, hippocampal HT-22 cells were treated with βhydroxybutyric acid at different doses to elucidate the neurotropic effects. In addition, markers of oxidative stress, mitochondrial function, and apoptosis were investigated. As a result, the ketone body (β-hydroxybutyric acid) showed a significant increase in hippocampal neuronal viability at a moderate dose. Results show that β-hydroxybutyric acid exhibited antioxidant effect by decreasing prooxidant oxidative stress markers such as reactive oxygen species, nitrite content, and increasing glutathione content leading to decreased lipid peroxidation. Results show that β-hydroxybutyric acid improved mitochondrial functions by increasing Complex-I and Complex-IV activities and showing that β-hydroxybutyric acid significantly reduces caspase-1 and caspase-3 activities. Finally, using computational pharmacokinetics and molecular modeling software, we validated the pharmacokinetic effects and pharmacodynamic (N-Methyl-D-aspartic acid and acetylcholinesterase) interactions of βhydroxybutyric acid. The computational studies demonstrate that β-hydroxybutyric acid can interact with N-Methyl-D-aspartic acid receptor and cholinesterase enzyme (the prime pharmacodynamic targets for cognitive impairment) and further validates its oral absorption, distribution into the central nervous system. Therefore, this work highlights the neuroprotective potential of ketone bodies in cognitive-related neurodegenerative diseases.

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Augmented oxidative stress and reduced mitochondrial function in ageing goat testis

Cited by 6 publications

References 43 publications

Cordycepin, a major bioactive component ofCordyceps militaris, ameliorates diabetes‐induced testicular damage through the Sirt1/Foxo3a pathway

Cordycepin, a major bioactive component ofCordyceps militaris, ameliorates diabetes‐induced testicular damage through the Sirt1/Foxo3a pathway

Evaluate the in vitro effect of anthracycline and alkylating cytophosphane chemotherapeutics on dopaminergic neurons

𝜷-hydroxybutyric acid attenuates oxidative stress and improves markers of mitochondrial function in the HT-22 hippocampal cell line

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