Spider silk protein, renowned for its excellent mechanical properties, biodegradability, chemical stability, and low immune and inflammatory response activation, consists of a core domain with a repeat sequence and non-repeating sequences at the N-terminal and C-terminal. In this review, we focus on the relationship between the silk structure and its mechanical properties, exploring the potential applications of spider silk materials in the detection of energetic materials.

Hexanitrohexaazaisowurtzitane (CL-20) is a high-energy-density material known for its exceptional explosive performance, but it suffers from significant safety concerns due to its high sensitivity. To mitigate this issue, researchers have explored the synthesis of CL-20-based cocrystals with other energetic materials to achieve a balance between energy output and safety. Recent advancements in CL-20 cocrystals have focused on developing novel synthesis methods and leveraging computational design techniques to predict and optimize their physicochemical properties. However, the toxicity of CL-20 cocrystals, along with their environmental and health risks, remains a critical concern. This review systematically examines recent progress in CL-20 cocrystal energetic materials, emphasizing toxicity profiles and mechanistic insights into their components. The findings serve as a foundation for the development of safer energetic materials, thereby facilitating sustainable advancements in manufacturing technologies and industrial applications of CL-20.

Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) is a globally recognized energetic material that widely used in industrial, mining, and military fields. Like hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) and other nitramine compounds, HMX has also been reported to exhibit neurotoxicity. However, the molecular mechanisms underlying the toxic effects of HMX remain poorly understood. Therefore, this study aims to investigate the neurotoxicity induced by HMX by adopting PC12 cells. The results show that HMX treatment decreased cell viability and upregulated the intracellular free calcium ions (Ca²⁺) in PC12 cells. Furthermore, HMX caused aggravated oxidative stress in PC12 cells, as evidenced by the upregulations of reactive oxygen species (ROS) and malondialdehyde (MDA). Intracellular biochemical assays demonstrated that HMX induced loss of mitochondrial membrane potential in PC12 cells. Notably, altered expression of brain-derived neurotrophic factor (BDNF) and ionotropic glutamate receptors (iGluRs), as well as an abnormal transcription profile, were also observed in PC12 cells treated by HMX. These findings suggest that HMX exerts toxic effects on PC12 cells, involved in oxidative stress, and disturbances in Ca²⁺ and BDNF, accompanied by aberrant iGluRs. Overall, the present study helps us better understand the health hazards associated with HMX and provides valuable insights for developing the health protection standards related to HMX exposure.

Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) is a nitramine explosive widely used in military and industrial fields. While emerging evidence suggests the neurotoxicity of HMX, the mechanisms underlying central nervous system (CNS) damage remain largely unknown. In the present study, we established a mouse model of 28-day subacute HMX exposure to explore HMX-induced neurotoxicity and underlying mechanisms in vivo. Behavioral assessments revealed that HMX increased spontaneous locomotor activity and central exploration in the open field test, and reduced immobility time in the forced swimming test, indicating abnormal emotional regulation. The Morris water maze further demonstrated impaired hippocampus-dependent spatial learning and memory in HMX-treated mice, as evidenced by prolonged platform latency. Histopathological analysis showed hippocampal demyelination in HMX-treated mice, accompanied by downregulation of myelin structural proteins (MBP, PLP1) and oligodendrocyte lineage proteins (OLIG2, CNPase). Additionally, proteomic analysis identified 173 differentially expressed proteins in the HMX-exposed hippocampus, which were enriched in myelination, synaptic transmission and neuroactive ligand–receptor interaction pathways. Collectively, our findings demonstrate that subacute HMX exposure induces behavioral deficits and demyelination in mice hippocampus, providing a novel mechanistic insight into HMX neurotoxicity and a theoretical basis for occupational health protection against HMX exposure.