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Rapid One-step Enzymatic Synthesis and All-aqueous Purification of Trehalose Analogues
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Primary study on the toxic mechanism of vanadyl trehalose in Kunming mice

Pingzhe Jiang1, Qiqi Liu1, Zaizhong Ni1

  • 1Key Laboratory for Bioactive Materials of the Ministry of Education, Institute of Molecular Biology, College of Life Science, Nankai University, 300071, Tianjin, China; State Key Laboratory of Medicinal Chemical Biology, Nankai University, 300071, Tianjin, China.

Regulatory Toxicology and Pharmacology : RTP
|January 7, 2018
PubMed

Insights

Vanadyl trehalose lowers blood glucose but causes stomach and intestinal toxicity in mice. Its toxicity mechanisms involve oxidative stress, inflammation, apoptosis, and gut microbiota disruption.

Area of Science:

  • Biochemistry
  • Toxicology
  • Microbiology

Background:

  • Vanadyl trehalose is investigated for its potential to lower blood glucose levels.
  • Previous studies indicate vanadyl trehalose may cause mild gastrointestinal toxicity in diabetic mice.
  • Understanding the toxicological mechanisms is crucial for assessing its therapeutic safety.

Purpose of the Study:

  • To elucidate the toxicological mechanisms of vanadyl trehalose in the stomach and intestine of Kunming mice.
  • To analyze changes in antioxidant levels, pro-inflammatory cytokine expression, apoptosis factors, and intestinal microflora.

Main Methods:

  • Oral administration of vanadyl trehalose to diabetic Kunming mice.
  • Analysis of oxidative stress markers (MDA, SOD, T-AOC).
  • Measurement of inflammatory factors (IL-1β, COX-2, TNF-α, iNOS).
  • Assessment of apoptosis factors (Bcl-2/Bax ratio, caspase-3).
  • Evaluation of intestinal microflora composition (Enterobacteriaceae, Enterococcus, Lactobacillus, Bifidobacterium).

Main Results:

  • Vanadyl trehalose administration led to elevated MDA and decreased SOD and T-AOC, indicating oxidative stress.
  • Increased expression of inflammatory factors (IL-1β, COX-2, TNF-α, iNOS) was observed.
  • Apoptosis factors showed a decreased Bcl-2/Bax ratio and increased caspase-3.
  • Intestinal microflora dysbiosis occurred, with increased Enterobacteriaceae and Enterococcus, and decreased Lactobacillus and Bifidobacterium.

Conclusions:

  • The toxicity of vanadyl trehalose in the stomach and intestine is linked to the activation of the oxidative stress system.
  • Increased inflammatory response and promotion of apoptosis contribute to vanadyl trehalose toxicity.
  • Disruption of the normal intestinal microflora is a key mechanism underlying vanadyl trehalose-induced toxicity.
Keywords:
Kunming miceToxic mechanismVanadiumVanadyl trehalose

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