Objective: To elucidate the impact of benzoquinone (BQ) on lipid homeostasis and cytotoxicity in Saccharomyces cerevisiae. Methods: The impact of BQ exposure on wild-type and knockouts of PC biosynthesizing genes revealed the alterations in the lipids that were analyzed by fluorescence microscopy, thin layer chromatography, and gene expression studies. Results: In yeast, BQ exposure reduced the growth pattern in wild-type cells. The gene knockout strains of the phospholipid metabolism altered the mRNA expression of the apoptosis genes – both caspase-dependent and independent. The BQ exposure revealed an increase in both the phospholipids and neutral lipids via the CDP:DAG and the Kennedy pathway genes. The accumulation of both neutral lipids and phospholipids during the BQ exposure was discrete and regulated by different pathways. Conclusions: BQ exposure inhibited cell growth, increased the reactive oxygen species (ROS), and altered membrane proliferation. The CDP:DAG and Kennedy pathway lipids also discretely altered by BQ, which is required for the membrane functions and energy purposes of life.

Benzene metabolites (HQ and BQ) are toxic compounds and their presence in human cause alteration in cellular respiration and kidney damage. In the current study, Saccharomyces cerevisiae has been used as a model organism and acute exposure of hydroquinone (HQ) decreased cell growth and increased reactive oxygen species (ROS). The expression of apoptosis regulatory genes (YCA1, NUC1, YSP1 and AIF1) were increased with HQ exposure in the wild-type cells. HQ exposure in the wild-type cells altered both the phospholipid and neutral lipid levels. Phosphatidylcholine is a vital membrane lipid that has a vital role in membrane biogenesis and was increased significantly with HQ. The neutral lipid results were supported with lipid droplets data and mRNA expression study. The phospholipid knockouts (Kennedy pathway) accumulated neutral lipids via the CDP-DAG (cytidine-diphosphate-diacylglycerol) pathway genes both in the presence and absence of HQ.

Hydroquinone (HQ) and benzoquinone (BQ) are known benzene metabolites that form reactive intermediates such as reactive oxygen species (ROS). This study attempts to understand the effect of benzene metabolites (HQ and BQ) on the antioxidant status, cell morphology, ROS levels and lipid alterations in the yeast Saccharomyces cerevisiae. There was a reduction in the growth pattern of wild-type cells exposed to HQ/BQ. Exposure of yeast cells to benzene metabolites increased the activity of the anti-oxidant enzymes catalase, superoxide dismutase and glutathione peroxidase but lead to a decrease in ascorbic acid and reduced glutathione. Increased triglyceride level and decreased phospholipid levels were observed with exposure to HQ and BQ. These results suggest that the enzymatic antioxidants were increased and are involved in the protection against macromolecular damage during oxidative stress; presumptively, these enzymes are essential for scavenging the pro-oxidant effects of benzene metabolites.