Impact of hypoxia on male reproductive functions

Oyedokun, P A; Akhigbe, R.E.; Ajayi, Lydia Oluwatoyin; Ajayi, Ayodeji Folorunsho

doi:10.1007/s11010-022-04559-1

Cited by 34 publications

(9 citation statements)

References 110 publications

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“…Hypoxia suppression of EGF signaling is conserved in other organisms (Deygas et al, 2018;Maxeiner et al, 2019), and altered expression of EGFR signaling components has been reported both in human populations living in high altitudes (Jha et al, 2016) and in Drosophila populations which have undergone multiple generations of selection for hypoxia tolerance (Zhou et al, 2008). Also, hypoxia can modulate steroidogenesis and steroid functions in many animals (Bera et al, 2020;Oyedokun et al, 2023;Wang et al, 2008;Yao et al, 2021), and diseases that can result in reduced systemic oxygen levels in humans -such as chronic obstructive pulmonary disease, sleep apnea or asthma -can impact steroid-induced development and sexual maturation (Drosdzol et al, 2007;Gaudino et al, 2021;Shaw et al, 2013). Thus, the mechanisms that we describe here in Drosophila may reflect more general mechanisms by which low oxygen can affect animal development.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia delays steroid-induced developmental maturation inDrosophilaby suppressing EGF signaling

Turingan

Tan

Wright

et al. 2023

Preprint

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Animals often grow and develop in unpredictable environments where factors like food availability, temperature, and oxygen levels can fluctuate dramatically. To ensure proper sexual maturation into adulthood, juvenile animals need to adapt their growth and developmental rates to these fluctuating environmental conditions. Failure to do so can result in impaired maturation and incorrect body size. Here we describe a mechanism by which Drosophila larvae adapt their development in low oxygen (hypoxia). During normal development, larvae grow and increase in mass until they reach critical weight (CW), after which point a neuroendocrine circuit triggers the production of the steroid hormone ecdysone from the prothoracic gland (PG), which promotes maturation to the pupal stage. However, when raised in hypoxia (5% oxygen), larvae slow their growth and delay their maturation to the pupal stage. We find that, although hypoxia delays the attainment of CW, the maturation delay occurs mainly because of hypoxia acting late in development to suppress ecdysone production. This suppression operates through a distinct mechanism from nutrient deprivation, occurs independently of HIF-1 alpha and does not involve modulation of PTTH, the main neuropeptide that initiates ecdysone production in the PG. Instead, we find that hypoxia lowers the expression of the EGF ligand, spitz, and that the delay in maturation occurs due to reduced EGFR/ERK signaling in the PG. Our study sheds light on how animals can adjust their development rate in response to changing oxygen levels in their environment. Given that hypoxia is a feature of both normal physiology and many diseases, our findings have important implications for understanding how low oxygen levels may impact animal development in both normal and pathological situations.

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Section: Discussionmentioning

confidence: 99%

Hypoxia delays steroid-induced developmental maturation inDrosophilaby suppressing EGF signaling

Turingan

Tan

Wright

et al. 2023

Preprint

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“…Testicular torsion damages testicular blood flow, resulting in venous overload, arterial blockage, ischemia, and necrosis if surgical intervention is delayed [ 6 , 7 ]. Impairment of testicular blood flow leads to hypoxia, which is associated with an oxygen concentration insufficient to maintain testicular homeostasis [ 40 , 41 ]. The testis is highly susceptible to hypoxia because it is a highly metabolic organ [ 41 ].…”

Section: Mechanisms Of Testicular I/r Injurymentioning

confidence: 99%

“…Impairment of testicular blood flow leads to hypoxia, which is associated with an oxygen concentration insufficient to maintain testicular homeostasis [ 40 , 41 ]. The testis is highly susceptible to hypoxia because it is a highly metabolic organ [ 41 ]. Hypoxia impairs oxygen and nutrient supplies to the testicular tissue.…”

Section: Mechanisms Of Testicular I/r Injurymentioning

confidence: 99%

“…Testicular hypoxia also results in enhanced prostaglandin E1 (PGE1) production that in turn overpowers tissue growth factor β1 (TGF β1), resulting in collagen deposition, and vascular dysfunction. Additionally, hypoxia upregulates vascular endothelial growth factor (VEGF), which triggers inhibition of germ cell proliferation and spermatogenic arrest [ 41 ].

Fig.…”

Section: Mechanisms Of Testicular I/r Injurymentioning

confidence: 99%

“…It has also been confirmed that hypoxia induces reactive oxygen species (ROS) generation via several pathways. Hypoxia down-regulates NRF-1 and initiates excessive generation of ROS, which in turn activates testicular and sperm cell lipid peroxidation, DNA damage and apoptosis [ 41 ]. Hypoxia-induced ROS generation may also be mitochondrial-dependent.…”

Section: Mechanisms Of Testicular I/r Injurymentioning

confidence: 99%

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Pathophysiology and management of testicular ischemia/reperfusion injury: Lessons from animal models

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Akhigbe

et al. 2024

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Hypoxia, NSAIDs, and autism: A biocultural analysis of stressors in gametogenesis

Burke

2024

American J Hum Biol

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Cultural and generational trends have increasingly favored “anti‐inflammatory” action, innovating a new class of analgesic, non‐steroidal anti‐inflammatory drugs (NSAIDs) in the 20th century. The modern human body has been molded over evolutionary time and while acknowledging inflammation can be pathologically entwined, it also serves an important role in healthy folliculogenesis and ovulation, shaping cues that drive needed vascular change. This review argues that because of anti‐inflammatory action, the cultural invention of NSAIDs represents a particular stressor on female reproductive‐age bodies, interacting with natural, underlying variation and placing limits on healthy growth and development in the follicles, creating potential autism risk through hypoxia and mutagenic or epigenetic effects. Since testes are analogs to ovaries, the biological grounding extends naturally to spermatogenesis. This review suggests the introduction of over‐the‐counter NSAIDs in the 1980s failed to recognize the unique functioning of reproductive‐age bodies, challenging the cyclical inflammation needed for healthy gamete development. NSAIDs are framed as one (notable) stressor in an anti‐inflammatory era focused on taming the risks of inflammation in modern human life.

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Impact of hypoxia on male reproductive functions

Cited by 34 publications

References 110 publications

Hypoxia delays steroid-induced developmental maturation inDrosophilaby suppressing EGF signaling

Hypoxia delays steroid-induced developmental maturation inDrosophilaby suppressing EGF signaling

Pathophysiology and management of testicular ischemia/reperfusion injury: Lessons from animal models

Hypoxia, NSAIDs, and autism: A biocultural analysis of stressors in gametogenesis

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