A new study by researchers at the Indian Institute of Technology Bombay has uncovered fresh insights into why some widely used antibiotics, despite being life-saving drugs, can sometimes trigger liver damage. The research, led by Prof Ashutosh Kumar from the Department of Biosciences and Bioengineering at IIT Bombay along with Prof Vetriselvan Subramaniyan of Sunway University, focuses on how certain antibiotics interact with liver cells at a microscopic level, potentially paving the way for safer drug design and improved prediction of adverse effects.
Antibiotics remain among the most important medical breakthroughs, routinely used to combat bacterial infections ranging from pneumonia and tuberculosis to post-surgical complications. However, clinicians have long observed that some antibiotics can elevate liver enzymes, cause inflammation or, in rare cases, precipitate severe drug-induced liver injury. Such reactions are often unpredictable and can escalate to acute liver failure, especially in vulnerable patients.
The new study shifts attention from the conventional explanation that toxicity is primarily dose-related or linked solely to chemical potency. Instead, the researchers examined how antibiotic molecules position themselves on the surface of liver cells and interact with the outer boundary known as the cell membrane. The liver, being the central organ for drug metabolism, is particularly exposed to high concentrations of medications and their breakdown products, making it susceptible to unintended damage.
According to the researchers, whose study was published in the latest edition of the ScienceDirect of Elsevier, the interaction between antibiotic molecules and the lipid-rich membrane of liver cells may play a crucial role in triggering stress responses within the cell. If a drug embeds itself in a way that disturbs membrane stability or alters its structure, it can set off a cascade of inflammatory signals or disrupt normal cellular functioning. Over time, this disturbance may contribute to elevated liver enzymes observed in routine blood tests or, in extreme cases, lead to tissue injury.
“Traditionally, people believed that a drug molecule's harm to cells comes from how much it ruptures the cell membrane. Our results can change that view,” says Prof. Kumar.
By studying these membrane-level interactions, the team proposes a framework that could help predict which antibiotic compounds are more likely to pose a risk to liver health. This approach moves beyond traditional toxicity testing, which often identifies problems only after damage has occurred in clinical settings or late-stage trials. A predictive model based on cell membrane interaction could enable pharmaceutical developers to screen candidate drugs earlier in the development cycle, potentially eliminating compounds with higher risk profiles before they reach patients.
The implications extend beyond antibiotics alone. Many classes of drugs are processed by the liver, and drug-induced liver injury remains one of the leading causes of medication withdrawal from global markets. A better understanding of how drugs physically and chemically interface with liver cell membranes could therefore reshape safety testing protocols across the pharmaceutical industry.
The study also underscores the growing role of interdisciplinary research, combining biosciences, bioengineering and biophysics to answer clinically relevant questions. By bridging laboratory findings with real-world medical concerns, the IIT Bombay–Sunway University collaboration highlights how fundamental cellular research can inform safer therapeutic innovation.
The researchers state in the report that this study suggests a new way to design safer medicines by focusing on how drugs interact with the fatty outer layer of cells. It also highlights the use of advanced computer models to predict possible side effects early in the drug development process, they say.
While antibiotics continue to save millions of lives each year, the findings serve as a reminder that even essential medicines carry biological trade-offs. With antibiotic resistance already posing a global threat, ensuring that these drugs are not only effective but also safer for long-term use is increasingly important. The researchers believe their work represents a step toward more rational drug design, where understanding how a molecule behaves at the cellular boundary becomes central to evaluating its overall safety profile.