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Autophagy01:27

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
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Enhanced autophagy reversed aflatoxin B1-induced decrease in lactate secretion of dairy goat Sertoli cells.

Shuaiqi Han1, Hongyun Zhang1, Xinyu Liu1

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Aflatoxin B1 (AFB1) impairs dairy goat Sertoli cells

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Area of Science:

  • Reproductive biology
  • Toxicology
  • Cellular metabolism

Background:

  • Aflatoxin B1 (AFB1) is a widespread food contaminant with known male reproductive toxicity.
  • The specific molecular mechanisms of AFB1 toxicity in testicular Sertoli cells (SCs) remain unclear.
  • SCs are crucial for germ cell development, providing essential support and nutrients.

Purpose of the Study:

  • To investigate the impact of AFB1 on lactate production and autophagy in dairy goat SCs.
  • To elucidate the role of autophagy in mitigating AFB1-induced effects on lactate secretion.

Main Methods:

  • Exposure of dairy goat SCs to AFB1.
  • Measurement of lactate production, ATP levels, and AMPK phosphorylation.
  • Analysis of autophagy activation (ULK1 phosphorylation) and expression of lactate transport proteins (GLUT1, GLUT3, LDHA, MCT4).

Main Results:

  • AFB1 significantly reduced lactate secretion, ATP levels, and AMPK phosphorylation in SCs.
  • AFB1 activated autophagy via AMPK-ULK1 signaling.
  • Enhanced autophagy partially restored lactate secretion by improving glucose utilization and increasing key protein expression.

Conclusions:

  • AFB1 disrupts the "Warburg-like" metabolism in dairy goat SCs, inhibiting lactate secretion essential for germ cell development.
  • Autophagy plays a protective role against AFB1-induced metabolic damage in SCs.