# Cell Response to Oxidative Stress in Antarctic Filamentous Fungi
## 7 Cold Stress Response of Antarctic Fungi and Adaptation
### Metabolic Adaptation Response  
In recent years, there has been a significant rise in the volume of research focused on the effect of low temperature on protein modifications through the application of proteomic methodologies [11]. Research conducted by [PERSON] et al. [155] on the proteomic profiles of fungi that inhabit black rocks under conditions of low-temperature stress demonstrated an increase in the total number of protein spots. The findings revealed significant changes in high molecular mass protein spots, particularly those ranging from 70 to 170 kDa, in the species _Friedmanniomyces endoliticus_ and _Conisopriorum perforans_. Conversely, the analysis of _Exophilia jeanselmei_ exhibited alterations in protein patterns at a lower molecular mass range of 25 to 100 kDa. Exposure of fungus _E. dermatitisidis_ to low-temperature stress resulted in a decline in proteins associated with metabolic activity, particularly those involved in general carbon metabolism. A comprehensive array of proteins engaged in energy metabolism pathways underwent down-regulation, encompassing malate synthase, malate dehydrogenase, acetyl-coenzyme A synthetase, and glyceraldehyde-3-phosphate dehydrogenase [219]. The proteomic study on the low-temperature stress response indicated a positive correlation between protein levels and transcription levels in certain pathways due to an increase in chaperones and energy metabolism pathways. As an illustration, a comparable modification in protein profiles was observed in response to both short-term and long-term low-temperature exposure to _Flammulina veltipes_[156]. Furthermore, [PERSON] et al. [154] demonstrated a substantial modification in the levels of various metabolic enzymes and ribosomal proteins in Antarctic isolates of _Pseudogymnoascus_ spp. Through pathway enrichment analysis, the authors further demonstrate diversity in the pathways associated with cold stress responses, particularly those related to metabolism and translation processes. Of interest are the studies conducted by [PERSON] et al. [183], which reported for the first time the involvement of tryptophan-based metabolic reprogramming in the response of _T. dupotti_ to cold stress. The response mechanisms of the psychrophilic strain _Mrakia psychrophilic_[182], _Flammulina veltipes_[156], and _Mortierella isbellina_[157] to low-temperature stress encompass several physiological changes. These include a desaturation of fatty acids, an accumulation of glycerol, an increase in the expression of glutamine synthetase and MFS transport proteins, and a decrease in the expression levels of citrate synthase, succinyl Co-A ligase, pyruvate decarboxylase, and ribosomal proteins. The impact of a significant reduction in growth temperature on carbon metabolism has been investigated in two Antarctic strains, one psychrotolerant and one mesophilic, along side a temperate mesophilic strain [165]. Findings indicated a pronounced elevation in the activity of hexokinase (HK), the enzyme that initiates glycolysis. A similar increase was noted for glucose-6-phosphate dehydrogenase (GPDH), which catalyzes the initial reaction in the pentose phosphate pathway (PPP), as well as glyceraldehyde 3-phosphate dehydrogenase (GAPDH), which plays a crucial role in energy production. A key conclusion drawn from this study is that low-temperature stress prompts a shift in carbohydrate metabolism from glycolysis toward the PPP, contributing to the survival mechanisms at suboptimal temperatures. Additionally, it is noteworthy that the enhancement in the activity of these three enzymes has been markedly more pronounced in cells during the exponential growth phase compared to those in the stationary phase. It should be noted that the short-term cold stress (4 \({}^{\circ}\)C) applied to Antarctic fungi _Penicillium_ sp. 161 and _A. glaucus_ 363 resulted in the re-routing of carbon metabolism away from glycolysis into the PPP, serving as a stress-resistance mechanism [220].