## 1 Introduction  
Mitochondria participate in numerous cellular processes being critical for cell survival and death. Besides their best-known function of ATP generation, the mitochondria are entirely involved in cellular metabolism, partly maintaining calcium homeostasis and regulating cell adaption to various stresses. They are implicated in ROS signaling modulation, maintenance of oxidative homeostasis, and apoptosis regulation under stress conditions [1, 2]. Indeed, mitochondria are involved in free radicals generation, with the respiratory chain as the leading ROS producer. Excessive ROS production is supposed to result from mitochondria dysfunction [3]. Mitochondria are indispensable organelles of any eukaryotic cell, determining the organism's fitness and physiology [4]. The damage of mitochondrial function is a universal sign of ageing in a eukaryotic cell [4; 5]. Some mechanisms causing damage to mitochondria bioenergetics include the accumulation of mutations and deletions in mtDNA, oxidation of mitochondria proteins, destabilization of macromolecular super-complexes in the respiratory chain, some changes in the lipid composition of the membranes, and modulation in mitochondria dynamics due to imbalance in organelle fusion, fission, and mitophagy [5]. The major ROS sources are mitochondrial respiratory chain, non-enzymatic reactions involving oxygen, phagocytosis, prostaglandin synthesis, the P450 cytochrome system, and ionizing radiation (in mammals). Thus, an increase in ROS generation due to an increased metabolic rate is considered the lifespan's principal determiner. Not only the abundant ROS generated in pathological mitochondria but also ROS produced in the normal ones can lead to oxidative damage of the cells causing the ageing process. The hypothesis known as the \"free radical theory\" of ageing (FRTA) [6] declares the major statements of ageing in any aerobes, which later result in the mitochondrial theory of ageing. The theory supposes that mitochondria are the primary ROS sources in a cell and consequently participate in ageing and lifespan regulation [7]. Nevertheless, some new data have led to a more thorough overview of mitochondria ROS function, which is now considered to be signaling molecules in numerous pivotal biological processes, including ageing and lifespan [8]. The molecular mechanisms of the response to oxidative stress and the role of ROS in ageing have been widely and keenly studied for a long time. Hence, using simple eukaryotic models, namely yeast organisms, can be helpful. The _Saccharomyces cerevisiae_ yeast is widely used in research on ageing mechanisms, and it contributes to understanding basic cellular and molecular processes [9]. Budding yeast research largely contributed to comprehending the ageing process and age-related diseases [10]. Yeasts, being the simplest unicellular eukaryotes, have many features in common with mammalian and human cells that permit studying both chronological and replicative ageing [11]. Moreover, the response of the yeast cell to oxidative stress is similar to that of mammals, including the sites of ROS generation in the electron transport chain and the performance of the major antioxidant enzyme complex [12]. Until recently, it was unknown if the composition of the mitochondrial membrane lipids during ageing in yeast can result in mitochondrial dysfunction. However, recent studies showed that in the _S. cerevisiae_ yeast, a metabolic pathway of ceramide and sphingolipid synthesis is an essential node of the signaling network to determine the replicative and chronological lifespan [13; 14; 15]. High content of triacylglycerlycerols (TAGs) is another aspect of lipid metabolism defining the lifespan of chronologically senescent yeast cells [15; 16]. The neutral lipids are synthesized in the endoplasmic reticulum (ER) and then accumulate into lipid bodies (Lb), which determines the longevity of senescent yeast cells regardless of any other signaling pathways [15].