The aim of the study was to verify the hypothesis that a potential cause of the phytotoxicity of diclofenac (DCF, a non-steroidal anti-inflammatory drug) is an effect of cell cycle progression. This research was conducted using synchronous cultures of a model organism, green alga Chlamydomonas reinhardtii. The project examined DCF effects on selected parameters that characterize cell cycle progression, such as cell size, attainment of commitment points, DNA replication, number of nuclei formed during cells division and morphology of cells in consecutive stages of the cell cycle, together with the physiological and biochemical parameters of algae cells at different stages. We demonstrated that individual cell growth remained unaffected, whereas cell division was delayed in the DCF-treated groups grown in continuous light conditions, and the number of daughter cells from a single cell decreased. Thus, the cell cycle progression is a target affected by DCF, which has a similar anti-proliferative effect on mammalian cells.

• Keywords
• Chlamydomonas reinhardtii, cell cycle, diclofenac, non-steroidal anti-inflammatory drug,
• MeSH
• Anti-Inflammatory Agents, Non-Steroidal toxicity   MeSH
• Cell Division drug effects   MeSH
• Cell Cycle drug effects   MeSH
• Chlamydomonas reinhardtii drug effects   genetics   growth & development   MeSH
• Diclofenac toxicity   MeSH
• DNA, Plant biosynthesis   genetics   MeSH
• Photosynthesis drug effects   MeSH
• DNA Replication drug effects   MeSH
• Cell Size drug effects   MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Anti-Inflammatory Agents, Non-Steroidal MeSH
• Diclofenac MeSH
• DNA, Plant MeSH