The effect of L-carnitine in reactive oxygen species reduction and apoptotic gene expression in mice after cyclophosphamide: An experimental study.

Almasi M; Shafiei G; Nikzad H; Karimian M; Moshkdanian G

doi:10.18502/ijrm.v22i8.17262

The effect of L-carnitine in reactive oxygen species reduction and apoptotic gene expression in mice after cyclophosphamide: An experimental study.

Almasi M, Shafiei G, Nikzad H, Karimian M, Moshkdanian G

International journal of reproductive biomedicine · 2024 · doi:10.18502/ijrm.v22i8.17262 · PMID:39494123 · PMC11528291

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This experimental study in 24 NMRI female mice examined whether L-carnitine (LC), given by intraperitoneal injections before and around cyclophosphamide (CP) exposure, could protect oocytes by reducing reactive oxygen species (ROS) and modulating apoptotic gene expression. After superovulation and collection of mature oocytes, ROS levels were quantified using DCFH-DA fluorescence, and mRNA expression of pro-apoptotic genes Bax and Caspase3 and anti-apoptotic Bcl2 was measured by RT-PCR; the authors state CP increased ROS and activated apoptosis-associated gene changes, while LC mitigated these effects. CP upregulated Bax and Caspase3 and decreased Bcl2, whereas LC reduced ROS and shifted gene expression toward lower Bax/Caspase3 and higher Bcl2, with LC+CP producing values not significantly different from control for ROS but showing gene-expression shifts relative to control as well. The main limitation is that only oocyte gene expression and ROS were assessed without direct measures of oocyte survival, developmental competence, or mechanistic causality beyond these readouts. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

BackgroundCyclophosphamide (CP), a utilized anticancer drug, is known to cause infertility in women. However, L-carnitine (LC), an antioxidant, has been shown to offer protective benefits against infertility.ObjectiveThis study aimed to evaluate the levels of reactive oxygen species (ROS) and apoptotic gene expression in mice treated with CP and LC.Materials and methods24 NMRI female mice (6-8 wk, 30 ± 5 gr) were divided into 4 groups: control group: received normal saline intraperitoneal (IP) injection for 10 days; CP group: received 75 mg/kg of CP as a single IP on the 10 th day of the experiment; LC group: received 200 mg/kg of LC IP for 10 days; LC+CP group: received LC for 10 days and CP single IP injection on the 10 th day of the experiment. After 10 days, mice were superovulated. The oviducts were then removed, and the oocytes of each group were collected for evaluating apoptotic gene expression B-cell lymphoma 2(Bcl2), Bcl2-associated X(Bax), and Caspase3 via real-time polymerase chain reaction and intracellular ROS levels by dichloro-dihydro-fluorescein diacetate fluorescence staining.ResultsData revealed that LC in the LC+CP group significantly increased Bcl2 gene expression (p = 0.01), and decreased Bax and Caspase3 gene expression compared to the CP group (p = 0.03, p = 0.04). LC decreased the ROS level in the LC+CP group compared to the CP group (p < 0.001).ConclusionFindings suggest that LC can scavenge the ROS caused by CP and modulate the apoptotic pathway via downregulating the Bax and Caspase3 genes and upregulating the Bcl2 gene in oocytes of mice exposed to CP.

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Gh. Moshkdanian, H. Nikzad, M. Almasi, and G. Shafiei had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Concept and design Gh. Moshkdanian, H. Nikzad, and M. Almasi. Acquisition, analysis, or interpretation of data Gh. Moshkdanian, H. Nikzad, M. Karimian, M. Almasi, and G. Shafiei. Drafting of the manuscript: M. Almasi, G. Shafiei, and M. Karimian. Critical revision of the manuscript for important intellectual content: All authors. Statistical analysis: M. Almasi, G. Shafiei, and Gh. Moshkdanian. Supervision: Gh. Moshkdanian and H. Nikzad.

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