Sugar and sucralose are frequently used together and separately in human food and beverages, which is the reason why studying their biological action on different organisms is really important. Nevertheless, the effect of highly concentrated sugar diet on male infertility is still under evaluation. The most important is that biological activity of sucralose, a chloroorganic synthetic sweetener, is highly persistent and difficultly altered in the environment, as its influence on the biological activity of other substances has not been completely elucidated yet. For this reason, in this work, sugar and sucralose–sugar mixtures, frequently used in beverages and other food products, influence Drosophila melanogaster behavior, longevity, reproductive performance, and genomic integrity is investigated. It has been demonstrated that an increase in sugar concentration promotes biological viability by enhancing prolificacy, lifespan, and locomotor performance. However, this only occurs up to a certain threshold concentration; beyond this, metabolic imbalance occurs. The presence of sucralose in solutions further augments the toxic effect, indicating high genotoxicity of the sweetener at doses over 0.5%, leading to significant DNA alterations and changing the Drosophila melanogaster behavior pattern. Therefore, either sugar or sucralose metabolic impact and toxicity is dose-related and their common presence in the solution might lead to the synergetic effect.

Bisphenol A is a synthetic compound widely used as a monomer in plastic and epoxy resins, whilst sucralose is an artificial sweetener frequently added to foods and beverages. Both substances can be detected in the environment and in food, making the assessment of their combined effects relevant from a food safety and public health perspective. The aim of this study is to investigate the biological and neurobehavioural implications of simultaneous exposure to BPA and sucralose in Drosophila melanogaster in vivo. The flies were distributed into two independent experiments: (BPA at 0.5, 1, 2, and 4 mM with a fixed sucralose molarity of 1.25 mM) and (sucralose at 6.3, 12.6, 25.1, and 50.3 mM with a fixed BPA molarity of 0.5 mM) compared to the control group (standard medium). Prolificacy, body weight, longevity, and negative geotaxis were evaluated in adults, whereas locomotor behavior and DNA integrity (Comet assay) were analyzed in L₃ larvae neuroblasts. The results revealed that the co-exposure to BPA and sucralose induces a significant reduction in prolificity at 0.5 mM BPA (50% at the highest concentrations), as well as in body weight and lifespan (54 days vs. 89 days in the control group); neurobehavioral tests revealed impaired locomotion, with a decrease in movement from 60 s in the control group to 0.67 s in treated larvae. DNA damage confirmed that exposure increases DNA strand breaks. This study provides pioneering in vivo evidence that BPA and sucralose together suggest combined toxicity leading to significant physiological homeostasis disruption. Future research should utilize genetic models with varying antioxidant defense capabilities to further define the metabolic variations in these combined exposures.

Tobacco smoke has been consistently associated with impaired spermatozoa quality in men, including decreased concentration, motility, and increased morphological abnormalities. Key tobacco-related toxins such as nicotine and cadmium induce oxidative stress, leading to DNA damage in germ cells. This study aimed to evaluate the effects of tobacco smoke exposure on male fertility using Drosophila melanogaster as an in vivo model. Fertility, fecundity, parental toxicity, lifespan, and spermatozoa morphology were assessed in two strains: the wild-type Oregon K and the DNA repair-deficient mus308. Males were exposed to whole-tobacco smoke in a controlled environment for periods of 0, 1 and 7 min. Tobacco smoke exposure reduced fertility, fecundity, and offspring longevity in both strains. Additionally, spermatozoa from mus308 males exhibited a higher frequency of morphological abnormalities. These findings demonstrate the detrimental impact of tobacco smoke on male reproductive function and suggest increased vulnerability in organisms with impaired DNA repair capacity.