Biochemical Basis of Drug Resistance

Introduction

Drug resistance is a major challenge in the treatment of various diseases, including cancer, bacterial infections, and HIV. It occurs when the microorganisms or cancer cells develop mechanisms to evade the effects of drugs, rendering them ineffective. Understanding the biochemical basis of drug resistance is crucial for developing new strategies to overcome this problem.

Mechanisms of Drug Resistance

There are several mechanisms by which microorganisms or cancer cells develop drug resistance. One common mechanism is the overexpression of drug efflux pumps, which actively remove the drug from inside the cell, reducing its concentration to subtherapeutic levels. Another mechanism is the alteration of drug targets, such as mutations in the target protein that prevent the drug from binding effectively. Additionally, some microorganisms develop metabolic pathways to detoxify the drug or repair the damage caused by it.

Genetic Basis of Drug Resistance

The genetic basis of drug resistance involves mutations in the genes responsible for drug transport, target proteins, or drug metabolism. These mutations can be acquired through random mutations or through horizontal gene transfer from other resistant microorganisms. The presence of resistance genes on plasmids or transposons allows for the rapid spread of drug resistance among bacterial populations.

Biochemical Pathways Involved in Drug Resistance

Several biochemical pathways are involved in drug resistance, including drug metabolism, DNA repair, and cell signaling pathways. For example, some drugs are metabolized by enzymes that are overexpressed in resistant cells, leading to increased drug detoxification. Additionally, mutations in DNA repair pathways can prevent the drug-induced damage from being repaired, allowing the cells to survive the drug treatment. Cell signaling pathways can also play a role in drug resistance by promoting cell survival and proliferation in the presence of the drug.