ATTENUATING PROPERTIES

Isoniazid is a widely used drug in tuberculosis treatment regimens. Its application in direct observed therapy short course ”(DOTS) along with other medications has been well documented to be efficacious and effective. However, since its introduction over 70 years ago, it has been found to possess adverse effects as the induction of neuropathies. There are estimates that as many as 10 % of patients receiving isoniazid will develop some form of neuropathy. Introduction of new medications to stop these neuropathies still pose a challenge. Pyridoxine (vitamin B6) is currently recommended with isoniazid therapy to avert induction of neuropathy. Although ,the potential of vitamin C as an antioxidant to prevent induced neuropathies has been suggested based on previous studies, the findings from this study were intended to contribute valuable insights into the potential therapeutic role of vitamin C as an adjuvant to mitigate neuropathic complications in isoniazid- based therapies. Using well-established animal models, we assessed the effects of vitamin C supplementation on the development and progression of some neuropathic symptoms induced by isoniazid administration. Male Wistar rats were divided into six groups: control, isoniazid-treated (800 mg/kg), and combination-treated; Isoniazid with vitamin C in low (7.5 mg/kg), medium (15 mg/kg), high (30 mg/kg) daily doses and isoniazid with pyridoxine (50 mg/kg). Behavioural assessments, including sensory and motor function tests, were conducted at the end of a seven day period to monitor the onset and severity of neuropathy. In conclusion, our findings revealed that isoniazid administration led to a significant decline in sensory and motor functions indicative of peripheral nerve damage. Vitamin C supplementation did not demonstrate a remarkable attenuation of these neuropathic manifestations. Rats co- administered with isoniazid and vitamin C did not exhibit any improvement in sensory and motor functions when compared with the control and standard therapy of pyridoxine. These results negate the potential neuroprotective effects of vitamin C against isoniazid-induced peripheral neuropathy