This research aims to investigate the adverse effects of ZnO NP on ovarian tissue and the follicular and menstrual cycle and the protective effects of l-arginine on the aforementioned tissues. 30 rats were divided into five groups. The first group was the control group. The second and fourth groups received 100 mg/kg and 200 mg/kg ZnO NP, respectively. The third and fifth groups received the same doses of ZnO NP as the second and fourth groups, respectively. However, the third and fifth groups received an additional dose of 1.3 gr/kg of LA amino acid. ZnO NP and LA are given intraperitoneal for 21 days. Blood samples from each rat and a part of the ovarium were collected to test for gene expression and histological analysis. Compared to levels of housekeeping gene β-actine, levels of apoptosis effectors such as Bax, Bcl, Caspase 3, and Caspase 9 were significantly increased in all groups. In groups that received doses of LA (three and five), atretic follicle size was smaller compared to groups that did not receive LA (two and four). In addition, in the third group, the secondary and primordial follicle's generated oocytes were smaller compared with groups two, four, and five. Compared with the control group, all groups experienced morphological degeneration of follicles and tissue. ZnO NP has inevitable, morphological, and physiological effects on the ovary and can detrimentally impact the tissue. LA can aid in the regeneration of the tissue and block damage induced by stress and toxicity.

Fatty-acid-hydroxylase-associated neurodegeneration (FAHN) is a rare neurodegenerative disorder caused by loss-of-function mutations in the FA2H gene, leading to impaired enzymatic activity and resulting in myelin sheath instability, demyelination, and axonal degeneration. In this study, we established a human in vitro model using neurons and oligodendrocytes derived from induced pluripotent stem cells (hiPSCs) of a FAHN patient. This coculture system enabled the investigation of myelination processes and myelin integrity in a disease-relevant context. Analyses using immunofluorescence and Western blot revealed impaired expression and localisation of key myelin proteins in oligodendrocytes and cocultures. FA2H-deficient cells showed reduced myelination, shortened internodes, and disrupted formation of the nodes of Ranvier. Additionally, we identified autophagy defects—a hallmark of many neurodegenerative diseases—including reduced p62 expression, elevated LC3B levels, and impaired fusion of autophagosomes with lysosomes. This study presents a robust hiPSC-based model to study FAHN, offering new insights into the molecular pathology of the disease. Our findings suggest that FA2H mutations compromise both the structural integrity of myelin and the efficiency of the autophagic machinery, highlighting potential targets for future therapeutic interventions.