Lycopene modulates cholinergic dysfunction, Bcl-2/Bax balance, and antioxidant enzymes gene transcripts in monosodium

Kadry Sadek1, Tarek Abouzed2, Sherif Nasr3

  • 1a Department of Biochemistry, Faculty of Veterinary Medicine, Damanhour University, Al-Buhiyra Governorate, Egypt.

Insights

Monosodium glutamate (MSG) causes neurotoxicity by increasing oxidative stress and apoptosis. Lycopene effectively protects brain tissue from MSG

Area of Science:

  • Neuroscience
  • Toxicology
  • Nutritional Biochemistry

Background:

  • Monosodium glutamate (MSG) is a widely used food additive.
  • Concerns exist regarding potential neurotoxic effects of MSG.
  • Antioxidants may offer protective benefits against neurotoxicity.

Purpose of the Study:

  • To investigate the neurotoxic effects of MSG on brain tissue.
  • To evaluate the neuroprotective potential of lycopene against MSG-induced toxicity.

Main Methods:

  • Wistar rats were divided into four groups: control, MSG-treated, lycopene-treated, and MSG + lycopene-treated.
  • Animals were treated for 30 days with specific doses of MSG and/or lycopene.
  • Biochemical markers of oxidative stress, antioxidant status, enzyme activities (ChE, CPK, LDH, GST, SOD, CAT), and apoptosis-related proteins (Bax, Bcl-2) were analyzed in brain and serum.

Main Results:

  • MSG administration significantly increased lipid peroxidation, altered antioxidant homeostasis, and elevated levels of ChE, CPK, LDH, GST, SOD, and CAT.
  • MSG also reduced glutathione content and induced apoptosis by upregulating Bax.
  • Lycopene treatment ameliorated these MSG-induced changes, decreasing oxidative stress markers, normalizing enzyme activities, restoring glutathione levels, and upregulating anti-apoptotic Bcl-2.

Conclusions:

  • MSG induces significant neurotoxic effects, including oxidative stress and apoptosis.
  • Lycopene demonstrates potent neuroprotective properties against MSG toxicity.
  • Lycopene alleviates MSG-induced neurotoxicity by inhibiting lipid peroxidation and apoptosis signaling pathways.