Leydig cell death is real and can be explained.
See here: Male Hypogonadism: Basic, Clinical, and Therapeutic Principles
By Stephen J. Winters Page 36
So you can understand this a little better inhibition of steroidogenesis eg taking steroids or something else to shut down the creation of testosterone by stopping the release of LH resulting in cell damage and death. Or by disruption of the hypothalamic–pituitary axis which happens every time you take steroids by shutting down LH production.Leydig Cell Toxicology
Several agents have been identified as Leydig cell toxicants, including ethanol, ethane 1,2 dimethanesulphonate (EDS), 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCCD), and steroid hormone receptor antagonists. These toxicants can damage Leydig cells in three ways: overstimulation or inhibition of steroidogenesis, induction of tumor formation, and promotion of cell death. Leydig cells are vulnerable to several toxins through direct actions and/or by disruption of the hypothalamic–pituitary axis. Toxicants, such as ethanol, interfere with Leydig cell steroidogenesis by interfering with LH secretion, LH receptor binding, intracellular signal transduction pathways, and steroidogenic enzyme activities. Ethanol, for example, decreases LH secretion and reduces LH receptor binding and intracellular cyclic guanosine 5′-monophosphate (GMP) levels. Hence, chronic alcohol abuse causes declines in testosterone levels (138–140). Tumor formation and cell death are also observed after toxicant exposures. Carcinogenesis is considered to be a consequence of multiple insults to the genome. Necrosis and apoptosis have both been implicated in the process of toxicant-related Leydig cell death, with ethylene dimethanesulfonate exposure as the experimental paradigm (141).
Chronic Effects of LH
LH also has long-term trophic effects on Leydig cells, requiring both transcription and increased translation of proteins. Chronic stimulation by LH is required for maintenance of Leydig cell steroidogenic enzyme levels and to support the steroidogenic organelle aparatus, including mitochondrial membrane potential and SER volume. Inhibition of LH action can be achieved by hypophysectomy (91–93), suppression of gonadotropins through steroid administration (94–96), and neutralization of LH or LH-releasing hormone (GnRH) by specific antibodies (97). LH blockade eliminates the chronic effects of this hormone, causing Leydig cell atrophy and loss of cellular volume, SER, steroidogenic enzyme activities (particularly P-45017α and P-450scc), LH receptor numbers, and the ability to secrete testosterone in response to LH (91,95).