Maize (Zea mays L.) is a vital crop worldwide, serving as a cornerstone for food security, livestock feed, and biofuel production. However, its cultivation is increasingly jeopardized by environmental challenges, notably soil salinization, which severely constrains growth, yield, and quality. To combat salinity stress, maize employs an array of adaptive mechanisms, including enhanced antioxidant enzyme activity and modulated plant hormone levels, which work synergistically to maintain reactive oxygen species (ROS) balance and ion homeostasis. This review explores the intricate interactions among ROS, antioxidant systems, plant hormones, and ion regulation in maize under salt stress, providing a comprehensive understanding of the physiological and molecular basis of its tolerance. By elucidating these mechanisms, this study contributes to the development of salt-tolerant maize varieties and informs innovative strategies to sustain agricultural productivity under adverse environmental conditions, offering significant theoretical insights into plant stress biology and practical solutions for achieving sustainable agriculture amidst global climate challenges.

Maize (Zea mays L.) is a vital crop worldwide, serving as a cornerstone for food security, livestock feed, and biofuel production. However, its cultivation is increasingly jeopardized by environmental challenges, notably soil salinization, which severely constrains growth, yield, and quality. To combat salinity stress, maize employs an array of adaptive mechanisms, including enhanced antioxidant enzyme activity and modulated plant hormone levels, which work synergistically to maintain reactive oxygen species (ROS) balance and ion homeostasis. This review explores the intricate interactions among ROS, antioxidant systems, plant hormones, and ion regulation in maize under salt stress, providing a comprehensive understanding of the physiological and molecular basis of its tolerance. By elucidating these mechanisms, this study contributes to the development of salt-tolerant maize varieties and informs innovative strategies to sustain agricultural productivity under adverse environmental conditions, offering significant theoretical insights into plant stress biology and practical solutions for achieving sustainable agriculture amidst global climate challenges.

Epidural analgesia (EA) may suppress the stress response or cortisol production during vaginal delivery by blocking pain transmission. However, there is no evidence that epidural analgesia contributes to epidural-related maternal fever (ERMF) by inhibiting the hypothalamic pituitary adrenal (HPA) axis. This study aimed to evaluate the relationship between maternal cortisol levels and ERMF during vaginal delivery. Prospective cohort study. The venous blood samples were collected from full-term pregnant women undergoing vaginal delivery and categorized into control group (<37.5 °C without EA), normal group (<37.5 °C with EA), mild group (37.5–37.9 °C with EA) or fever group (≥38 °C with Epidural analgesia (EA)). Then, plasma cortisol and pro-inflammatory cytokine levels (IL-6, TNF-α, IL-2 and IFN-γ) were assessed to determine the impact of EA on the stress response. We also detected hormones related to the HPA axis, including CRH and ACTH plasma concentration. Additionally, general adrenal function was evaluated by measuring renin, aldosterone, testosterone, and DHEA-s concentrations in the maternal venous blood. Clinical evidence of adrenal dysfunction was also investigated using medical records. Epidural analgesia induced high levels of cytokines IL-6 and TNF-α in all parturients, but ERMF was observed only in those with lower cortisol levels. Correlation analysis revealed a positive relationship between IL-6 (or TNF-α) and cortisol concentration ratio and maximum maternal temperature. Elevated ACTH, β-endorphin and αMSH levels were observed in parturients with ERMF, indicating primary adrenal dysfunction. Medical records showed no significant differences in symptoms, signs, or laboratory results related to adrenal function among the four groups. There was a relationship between relatively low maternal cortisol levels and ERMF. ChiCTR2200058359 obtained on April 7, 2022.

Epidural analgesia (EA) may suppress the stress response or cortisol production during vaginal delivery by blocking pain transmission. However, there is no evidence that epidural analgesia contributes to epidural-related maternal fever (ERMF) by inhibiting the hypothalamic pituitary adrenal (HPA) axis. This study aimed to evaluate the relationship between maternal cortisol levels and ERMF during vaginal delivery. Prospective cohort study. The venous blood samples were collected from full-term pregnant women undergoing vaginal delivery and categorized into control group (<37.5 °C without EA), normal group (<37.5 °C with EA), mild group (37.5–37.9 °C with EA) or fever group (≥38 °C with Epidural analgesia (EA)). Then, plasma cortisol and pro-inflammatory cytokine levels (IL-6, TNF-α, IL-2 and IFN-γ) were assessed to determine the impact of EA on the stress response. We also detected hormones related to the HPA axis, including CRH and ACTH plasma concentration. Additionally, general adrenal function was evaluated by measuring renin, aldosterone, testosterone, and DHEA-s concentrations in the maternal venous blood. Clinical evidence of adrenal dysfunction was also investigated using medical records. Epidural analgesia induced high levels of cytokines IL-6 and TNF-α in all parturients, but ERMF was observed only in those with lower cortisol levels. Correlation analysis revealed a positive relationship between IL-6 (or TNF-α) and cortisol concentration ratio and maximum maternal temperature. Elevated ACTH, β-endorphin and αMSH levels were observed in parturients with ERMF, indicating primary adrenal dysfunction. Medical records showed no significant differences in symptoms, signs, or laboratory results related to adrenal function among the four groups. There was a relationship between relatively low maternal cortisol levels and ERMF. ChiCTR2200058359 obtained on April 7, 2022.

No description available