Ameloriate Effect of Glucose Monohydrate on Nicotine Sulfate-Induced Toxicity and Teratogenicity in Xenopus Embryos: an Experimental Study

Abstract

It is well documented that nicotine causes low birth weight, preterm birth, pregnancy difficulties, lower fertility, inhibition of spermatogenesis, and decreased steroidogenesis and potassium channels conductance of Xenopus oocytes. Lung cancer is the most well-known adverse impact of nicotine. This work used a 96-hour FETAX test to examine how concurrent administration of glucose monohydrate modifies the effects of exposure to nicotine, nicotine sulfate, and/or glucose on ion channels and membrane potential in Xenopus leavis embryos at an early stage of development. In-vitro fertilised embryos were treated with nicotine and glucose alone or in combination for this aim, and the effects of those treatments were then assessed for potential teratogenic effects. At the conclusion of the FETAX technique, the ratios of healthy, abnormal, and dead embryos were calculated, and the length of embryos in each treatment group was assessed. The ratios of abnormal and dead embryos were considerably higher with nicotine treatment alone compared to controls. Compared to the results of the nicotine-alone treatment group, the ratio of aberrant embryos was marginally reduced by concurrent glucose and nicotine therapy. In contrast, the ratio of normal embryos was raised. Additionally, treatments with glucose, nicotine, and Nic+Glu significantly altered the resting membrane potentials of fertilised oocytes (p < 0.001). Our findings indicated that the simultaneous treatment groups that also received glucose had a protective impact on embryos. Such structured, more sophisticated research is required to confirm these findings.