ABSTRACT
Objective: To investigate the larvicidal activity of Syzygium guineense (Myrtaceae) (S. guineense), Monodora myristica and Zanthoxylum heitzii (Rutaceae) (Z. heitzii) ex-tracts against Aedes albopictus (Ae. albopictus). Methods: The larvicidal activity of the hydro-ethanolic extracts from these plant species was assessed at three different concentrations (50, 100 and 200 mg/L) on first-instar of Ae. albopictus larvae in comparison with untreated controls. Mortality rate was recorded daily for a period of 12 days. The values of LC50 and lethal time killing 50%of the tested individuals (LT50) were calculated using the log-probit analysis. Results: The root extract of S. guineense exhibited the best activity with 100%mortality after 8 days of treatment at 200 mg/L, followed by the fruit extract of Z. heitzii with 83.33%mortality at the same concentration. Nonetheless, larvae were most susceptible to the fruit extract of Z. heitzii both in terms of LC50 (39.89 mg/L) and LT50 (145.68 h). A statistically significant difference between the control and the group treated at 200 mg/L was noticed in all the extracts. Conclusions: The present study shows that the hydro-ethanolic extracts of S. guineense, Monodora myristica and Z. heitzii tested have significant larvicidal activity. These pre-liminary results are of great interest and some of these plant species can be proposed for the formulation of new bioinsecticides to control Ae. albopictus populations.
ABSTRACT
Objective/background: Tuberculosis [TB] is a worldwide public health problem. It is a contagious and grave disease caused by Mycobacterium tuberculosis. Current drugs such as isoniazid, pyrazinamide, and rifampicin used for the treatment of tuberculosis are potentially hepatotoxic and can lead to drug hepatitis. In order to improve the follow-up of TB patients in Cameroon, we carried out a study which aimed to evaluate the hepatotoxicity risk factors associated with anti-TB drugs
Methods: The studies were performed on 75 participants who had visited the Loum District Hospital located in the littoral region of Cameroon for their routine consultation. Participants have been selected based on pre-established criteria of inclusion and exclusion. Prior to the informed consent signature, patients were given compelling information about the objective and the result output of the study. They were questioned about antioxidant food and alcohol consumption as well as some clinical signs of hepatotoxicity such as fever, nausea, vomiting, and tiredness. The collected blood was tested for the determination of biochemical markers [transaminases and C-reactive protein] using standard spectrophotometric methods
Results: Biochemical analysis of samples showed a significant increase [p < .05] of aspartate aminotransferase and alanine aminotransferase values in TB patients coinfected with human immunodeficiency virus/AIDS [33.28 +/- 16.58 UI/L and 30.84 +/- 17.17 UI/L, respectively] compared with the respective values of the controls [16.35 +/- 5.31 UI/L and 16.45 +/- 4.83 UI/L]. Taking individually, the liver injury patient percentage of TB patients was significant compared to TBC when considering alanine aminotransferase and aspartate aminotransferase parameters. When considering risk factors, antioxidant food consumption significantly reduced the liver injury patient percentage for the above parameters, whereas an opposite situation was observed with alcohol consumption between TB-coinfection and TB patients. Regarding the C-reactive protein results, the percentage of positive tests was very high among coinfected patients [40%] compared with the control [15%]. The interactions between parameters related to alcohol consumption and intake of antioxidant foods showed a slight decrease in activity compared with interactions without food
Conclusion: The results showed that human immunodeficiency virus status and alcohol consumption constitutes aggravating factors for the occurrence of hepatic toxicity. In addition, the consumption of antioxidant foods simultaneously with TB drugs help in reducing the hepatotoxic effects of these drugs