Studying organelles in isolation has been proven to be indispensable for deciphering the underlying mechanisms of molecular cell biology. However, observing organelles in intact cells with the use of microscopic techniques reveals a new set of different junctions and contact sites between them that contribute to the control and regulation of various cellular processes, such as calcium and lipid exchange or structural reorganization of the mitochondrial network. In recent years, many studies focused their attention on the structure and function of contacts between mitochondria and other organelles. From these studies, findings emerged showing that these contacts are involved in various processes, such as lipid synthesis and trafficking, modulation of mitochondrial morphology, endoplasmic reticulum (ER) stress, apoptosis, autophagy, inflammation and Ca ${}^{2+}$ handling. In this review, we focused on the physical interactions of mitochondria with the endoplasmic reticulum and plasma membrane and summarized present knowledge regarding the role of mitochondria-associated membranes in calcium homeostasis and lipid metabolism.

Epidemiological studies continue to support the premise that diets rich in fruits and vegetables may offer protection against cancer of various anatomic sites. This correlation is quite persuasive for vegetables including Allium (e. g., garlic) and cruciferous (e. g., broccoli and watercress) vegetables. The bioactive food components responsible for the cancer chemopreventive effects of various edible plants have been identified. For instance, the anticancer effects of Allium and cruciferous vegetables are attributed to organosulfur compounds (e. g., diallyl trisulfide) and isothiocyanates (e. g., sulforaphane and phenethyl isothiocyanate), respectively. Bioactive food components with anticancer activity are generally considered to be antioxidants due to their ability to modulate expression/activity of antioxidative and phase 2 drug-metabolizing enzymes and scavenging free radicals. At the same time, more recent studies have provided convincing evidence to indicate that certain dietary cancer chemopreventive agents cause generation of reactive oxygen species (ROS) to trigger signal transduction culminating in cell cycle arrest and/or programmed cell death (apoptosis). Interestingly, the ROS generation by some dietary anticancer agents is tumor cell specific and does not occur in normal cells. This review summarizes experimental evidence supporting the involvement of ROS in cellular responses to cancer chemopreventive agents derived from common edible plants. AITC:allyl isothiocyanate ARE:antioxidant response element BITC:benzyl isothiocyanate DAS:diallyl sulfide DADS:diallyl disulfide DATS:diallyl trisulfide DR5:death receptor 5 ERK:extracellular signal-regulated kinase ITCs:isothiocyanates JNK:c-Jun N-terminal kinase MMP:mitochondrial membrane potential NAC:N-acetylcysteine OSCs:organosulfur compounds PEITC:phenethyl isothiocyanate ROS:reactive oxygen species SAC:S-allylcysteine SAMC:S-allylmercaptocysteine

Melatonin (Mel) is the major biologically active molecule secreted by the pineal gland. Mel and its metabolites, 6-hydroxymelatonin (6(OH)Mel) and 5-methoxytryptamine (5-MT), possess a variety of functions, including the scavenging of free radicals and the induction of protective or reparative mechanisms in the cell. Their amphiphilic character allows them to cross cellular membranes and reach subcellular organelles, including the mitochondria. Herein, the action of Mel, 6(OH)Mel, and 5-MT in human MNT-1 melanoma cells against ultraviolet B (UVB) radiation was investigated. The dose of 50 mJ/cm² caused a significant reduction of cell viability up to 48%, while investigated compounds counteracted this deleterious effect. UVB exposure increased catalase activity and led to a simultaneous Ca⁺⁺ influx (16%), while tested compounds prevented these disturbances. Additional analysis focused on mitochondrial respiration performed in isolated mitochondria from the liver of BALB/cJ mice where Mel, 6(OH)Mel, and 5-MT significantly enhanced the oxidative phosphorylation at the dose of 10⁻⁶ M with lower effects seen at 10⁻⁹ or 10⁻⁴ M. In conclusion, Mel, 6(OH)Mel and 5-MT protect MNT-1 cells, which express melatonin receptors (MT1 and MT2) against UVB-induced oxidative stress and mitochondrial dysfunction, including the uncoupling of oxidative phosphorylation.