Protective role of Lycopene against Aroclor 1254-induced changes on GLUT4 in the skeletal muscles of adult male rat

Abstract

Aroclor 1254 is the commercial mixture of highly toxic environmental pollutant, polychlorinated biphenyls (PCBs). Being immensely durable, it is extensively used and widely distributed. Studies show that Aroclor 1254 causes a variety of adverse health effects through free radical generation. The present investigation was designed to check the effect of Aroclor 1254 on the glucose transporter protein, GLUT4, which plays a key role in glucose homeostasis. The protective role of lycopene against the adverse effect of Aroclor 1254 was also tested. Group 1 rats received corn oil as vehicle and served as control. Groups 2, 3, and 4 were administered with Aroclor 1254 [2 mg kg⁻¹ body weight (b.w.) day⁻¹] intraperitoneally for 30 days. Groups 3 and 4 received lycopene (2 and 4 mg kg⁻¹ b.w. day⁻¹, respectively) orally in addition to Aroclor 1254. After 30 days, animals were euthanized and the skeletal muscles were dissected to determine the following parameters: GLUT4 messenger RNA (mRNA), GLUT4 protein (both plasma membrane and cytosolic fractions), and ¹⁴C-2-deoxyglucose uptake. Though there was no change in GLUT4 mRNA and fasting plasma glucose levels, Aroclor 1254 significantly decreased the GLUT4 protein level in both the subcellular fractions of the gracilis and triceps muscles. Most important, ¹⁴C-2-deoxyglucose uptake showed a significant decrease in Aroclor 1254 alone treated rats, and Aroclor 1254 plus 4 mg lycopene supplementation treatment maintained the same at par with control. Thus, Aroclor 1254 has adverse effects on GLUT4 translocation and ¹⁴C-2-deoxyglucose uptake, and lycopene administered along with Aroclor 1254 has a protective role over it.

Keywords::

• ¹⁴C-2-deoxyglucose uptake
• oxidative stress
• glucose
• antioxidant
• insulin signal transduction

Acknowledgments

The authors acknowledge the animal house staff, department office staff, and friends for their constant support and help. Above all, the authors humbly thank God Almighty who let us explore a small part of His creation.

Declaration of interest

The authors gratefully acknowledge a “University Research Fellow” scholarship (UGC-SAP-DRS-II) and the DST-FIST program for their financial support.

Notice of Correction

The version of this article published online ahead of print on 5 October 2012 contained errors in the author names. All author names have been corrected for this version.