Abstract
Millions of TB and HIV patients are treated with drugs that have toxic side effects. AZT, an inexpensive nucleotide reverse transcriptase inhibitor used in highly active anti-retroviral therapy T, is associated with mitochondrial oxidative stress and DNA damage. Isoniazid (INH), a first line antibiotic used to treat or prevent tuberculosis, alters liver function in ~20% of patients and is fatal in 1%-2%. Toxic intermediates of INH in the liver deplete glutathione and oxygen radical scavenging enzymes. The resulting increase in free radicals can irreversibly damage mitochondria and mitochondrial DNA (mtDNA). We are investigating AZT and INH dependent mtDNA damage in cultured human liver cells, as well as whether palm fruit juice (PFJ), an extract rich in polyphenols from the fruit of the oil palm (Elaeis guineensis), mitigates such damage.