Effect of rifampicin on the lipid profile of albino rats

The study was designed to investigate the effect of rifampicin on the lipid profile and histopathology of the heart of albino rats. Albino rats (42) were used and rifampicin was administered at 1.10mg/120g body weight (BW) and 0.55mg/120g BW for intervals of 20, 40 and 60days. Result from the study revealed that there was a significant increase (p<0.05) in triglyceride level for animals dosed with 1.10mg/120g BW 1.08±0.07, 1.37±0.12 and 1.52±0.12 mmol/L for 20, 40 and 60days of drug administration respectively when compared to the control (0.78±0.09 mmol/L ). Also there was a significant increase (p<0.05) in triglyceride level for those dosed with 0.55mg/120g BW 1.20±0.09, 1.46±0.09 and 1.47±0.01 mmol/L respectively for intervals of 20, 40 and 60days. There was also a significant increase P<0.05) in total cholesterol level for animals dosed with 1.10mg/120g BW ie 1.85±0.10, 2.08±0.15, and 2.10±0.18 mmol/L for 20, 40 and 60 days respectively and animals dosed with 0.55mg/120g BW ie 1.83±0.15, 2.03±0.12 and 2.05±0.10 mmol/L for 20, 40 and 60 days respectively when compared to the control (1.40±0.06 mmol/L ). There was a significant decrease in the high density lipoprotein-cholesterol level of animals dosed with 1.10mg/120g BW for 20, 40 and 60 days respectively (0.37±0.08, 0.45±0.08 and 0.45±0.10 mmol/L) and also in animals dosed with 0.55mg/120g BW (0.40±0.09, 0.42±0.07 and0.40±0.06 mmol/L) for 20, 40 and 60 days respectively, when compared to the control value (0.68±0.07 mmol/L) at (p<0.05). Histological examination of the heart revealed normal architectural structure of the heart after rifampicin administration for 20 and 60days, though pattern of plasma lipid alteration suggests dyslipidemia; therefore plasma lipid profile should be monitored routinely because of the positive relationship between increased dyslipidemia with cardiovascular diseases. © JASEM Tuberculosis or TB (short for tubercle bacillus) is a common and potentially lethal infectious disease caused by various strains of mycobacteria, usually in humans (kumar et al., 2007). It is caused by a rod shaped bacterium named Mycobacterium tuberculosis (MTB). It was first isolated in 1882 by a German physician named Robert Koch who received the Nobel Prize for this discovery. Tuberculosis usually attacks the lungs but can also affect other parts of the body (Kumar et al., 2007). It is spread through the air when people who have an active MTB infection cough, sneeze, or otherwise transmit their saliva through the air (Konstantinos, 2010). Most infections in humans result in an asymptomatic, latent infection, and about one in ten latent infections eventually progresses to active disease, which, if left untreated, kills more than 50% of its victims (Konstantinos, 2010). An estimated 1.7 million people died from TB in 2009. The highest number of deaths was in the Africa Region. Nigeria has the world’s fourth largest tuberculosis (TB) burden, with more than 460,000 estimated new cases in 2007. Since 2002, DOTS (the internationally recommended strategy for TB control) coverage has increased rapidly from 55 percent in 2002 to 91 percent 2007, and subsequently, case detection and notification of all forms of TB more than doubled from 38,628 in 2002 to 86,241 in 2006. Although still far short of WHO’s target of 70 percent, the TB case detection rate increased from 11 percent in 2002 to 23 percent in 2007. The public health burden posed by TB is becoming increasingly important as the country’s HIV/AIDS epidemic unfolds. WHO estimates that more than a quarter of new TB patients are HIV positive? Collaborative TB-HIV/AIDS services are being scaled up and the number of TB patients tested for HIV increased from about 7,500 in 2006 to 27,850 in 2007, or about one-third of all notified cases. The National TB and Leprosy Control Program (NTBLCP) coordinates and provides strategic direction for TB control activities in Nigeria. The Federal Ministry of Health declared TB a national emergency in April 2006 and inaugurated the Effect of rifampicin on the lipid 134 PETERS, D.E : ICHIPI-IFUKOR, R. N. National TB -HIV/AIDS Working Group in June 2006. Tuberculosis is the leading cause of death among HIV infected people in Africa. It is estimated that one third of the 40 million people living with HIV/AIDS worldwide are co-infected with TB. The primary treatment for mycobacteria is specific chemotherapy. For centuries, tuberculosis was a major killer disease but the introduction in the 1960s of rifampicin revolutionized therapy and tuberculosis came to be seen as an easily treated disease. Unfortunately, Mycobacterium tuberculosis has undergone rapid mutations and strains with increased virulence or multidrugs resistance are now common. This has restored tuberculosis to the status of a major health threat (Rang et at., 2007).The first line agents for treatment of tuberculosis are isoniazid (INH), rifampicin, pyrazinamide and ethambutol. Rifampicin with molecular formula and molecular weight of C43H58N4O12 and 822.96 respectively is a semisynthetic derivative of rifamycin, an antibiotic produced by Streptomyces mediterrenei. It acts by binding to and inhibiting DNA-dependent RNA polymerase in prokaryotic but not in eukaryotic cells. It enters phagocytics cells hence it can kill tubercle bacilli. (Geo et al.,2010). Rifampicin causes cholestasis at both the sinusoids and canaliculi of the liver because of defect in uptake by hepatocytes and defect in excretion respectively (Haddad, 1983). Hepatitis occurs in 1% or less of patients, and usually in the patient with pre-existing liver disease. Hypersensitivity reactions may occur, usually characterized by a "flu" type syndrome. Rifampicin may affect mammalian mitochondrial RNA synthesis at a concentration that is 100 times higher than that which affects bacterial RNA synthesis (Molavi, 1990). It has been suggested that some of these adverse effects associated with rifampicin may be attributed to its metabolite diacetyl rifampicin. This is lipid soluble, and thus can reach and kill intracellular, as well as extracellular, Mycobacteria. The effects of rifampicin on lipid profile in albino rats is the aim of this work. MATERIALS AND METHODS Source of experimental animals: Forty two (42) albino rats were purchased from the Department of Human Physiology, University of Nigeria Enugu Campus (UNEC) and acclimatized for one week at the Animal House of Biochemistry Department, University of Port Harcourt located at the botanical garden Choba Park. During acclimatization, the animals were fed with rat pellets and water ad