## 1 Introduction  
Cancer is one of the leading causes of death worldwide, characterized by the uncontrolled division and proliferation of cells due to genetic and environmental factors, ultimately leading to tumor formation [1; 2]. Over 100 types of cancer affect the human body, and different treatment methods are applied for each type of cancer, one of which is cytotoxic (chemotherapy) treatment. Although this method is effective for treating many types of cancer, it causes numerous side effects in the body. These side effects primarily affect rapidly dividing cells such as blood cells, gastrointestinal system cells, hair follicles, and reproductive organs. While cytotoxic chemotherapy used in cancer treatment achieves successful results in prolonging survival, it significantly reduces post-treatment quality of life, particularly due to its devastating effects on female reproductive health. Therefore, developing new approaches to mitigate the side effects of cisplatin is critically important. When cytotoxic chemotherapy is applied to premenopausal women, it can lead to follicular destruction, ovarian fibrosis, premature ovarian failure, reduced estrogen and progesterone levels, and an increased risk of infertility [3; 4]. The likelihood of infertility is associated with factors such as the patient's age, drug dosage, treatment duration, and combinations of cytotoxic chemotherapy agents [3; 5]. These drugs are also known to be both teratogenic (causing abnormalities in exposed fetuses) and mutagenic (inducing mutations in genetic material), thereby possessing a high potential for adverse effects [5; 6; 7]. Cytotoxic chemotherapy, with cisplatin (Cis, cis-diamminedichloroplatinum-II) being one of the most commonly used agents, is effectively utilized in various types of cancers, including head and neck, testicular, ovarian, bladder, and small-cell lung cancers [8; 9]. Although the exact mechanism of cisplatin's toxic effects on the ovaries remains unclear, it is suggested that increased production of reactive oxygen species and decreased antioxidant levels contribute to its toxicity [10; 11]. The effects of chemotherapy on the female reproductive system include oocyte damage and apoptosis around follicles, which may lead to premature ovarian failure [12]. Cisplatin can cause double-strand DNA damage, triggering apoptosis in granulosa cells and oocytes, thereby negatively impacting the follicular reserve in women. This highlights the critical need for innovative strategies to protect reproductive reserves during chemotherapy [13]. Numerous studies suggest that antioxidant therapy has the potential to prevent cisplatin-induced ovarian toxicity and the infertility resulting from this toxicity. Notably, mesenchymal stem cells (MSCs) have garnered significant attention in recent years due to their therapeutic capabilities and roles in damage repair. Multipotent stem cells derived from human umbilical cords (huMSCs) offer several advantages, including high self-renewal capacity, low immunogenicity, ease of accessibility, and wide availability [14]. Additionally, it has been demonstrated that huMSCs enhance ovarian reserve function [15]. Exosomes secreted by MSCs play a critical role in tissue regeneration and repair processes, as supported by numerous studies [16]. These exosomes exhibit functions such as reducing inflammation, modulating immune responses, and supporting tissue repair. Moreover, exosomes are reported to carry miRNAs that may influence cancer suppression or progression without posing a tumor formation risk [16; 17; 18]. Given these advantages, exosomes are considered a suitable option for clinical applications due to their low immunogenicity, lack of tumorigenic potential, and minimal ethical risks, making them a favorable alternative in therapeutic settings [15]. A review of the literature reveals that the effects of cisplatin on ovarian morphology have been examined in many studies. [PERSON] et al.