Exposure to many chemical agents such as drugs can cause hemolysis of red blood cells and can cause hemolytic anemia. The aim of this study is to investigate the hemolytic effect of Isoniazid. This experimental study was done on 40 adult Wistar rats. Animals were divided randomly into 3 groups. Control group: This group received only enough food and water. Reference group: This group received Solvent Isoniazid (physiology serum). The Experimental group received Isoniazid with 50 mg/kg dose of the animal weight for 14 days. Blood samples were applied to measure various parameters such as hematocrit level, hemoglobin level, red blood cells number, the red blood cell fragility. For evaluating the osmotic fragility sensitivity, red blood cells were incubated at 37 ° C at different concentrations of NaCl for 30 min and the extent of hemolysis was measured by colorimetric solution. Hemolysis was expressed based on the percentage of hemolysis of red blood cells in the presence of distilled water (100% hemolysis). The results showed a significant decrease in hemoglobin and hematocrit levels in the Isoniazid receiving group. However, Red blood cell count didn’t show any significant change. Furthermore, osmotic fragility test showed increased fragility of red blood in experimental group. In conclusion, Isoniazid cause to Hemoglobin degradation and prevent hemoglobin synthesis. But based on osmotic fragility test, Isoniazid can induce oxidative stress and RBC lysis at higher dose.

Isoniazid (INH) as the most important first order antituberculosis medication, should be present in all treatment regimens. Peripheral neuropathy (PNP) due to disturbance of pyridoxine metabolism is one of the most common side effects of this drug. In our study, 70 cases with active tuberculosis (Pulmonary & extrapulmonary ) at least for 2 months on Isoniazid without other risk factors for PNP were selected. Non of them were receiving pyridoxine supplement. They were 32 women and 38 men between 12- 67 years old. Nerve conduction velocity (NCV) and amplitude were measured in median and tibial motor nerves, also in ulnar and sural sensory nerves.Total incidence of PNP was 27 % and the most commonly involved nerves (in decreasing order) were sural 22. 8 % , ulnar 20% , tibial 17. 1% and median 5.7%. Therefore INH- Induced PNP is predominantly sensory and involves lower extremities more than upper ones. Axonal damage was the most common cause of PNP. 73. 6% of patients had involvement of more than one nerve. Only 15% of patients were symptomatic that indicates delayed appearance of clinical, compared to electrophysiological findings.

Background and the purpose of the study: Layer-by-layer (LbL) deposition of polyelectrolytes (PEs) has received a great attention in the area of drug delivery due to its simplicity and versatility. This research was aimed to develop multilayered microcapsules through LbL deposition of chitosan (CHI) and sodium alginate (NaALG) and utilize them as vehicle for controlled delivery of Isoniazid (INH).Methods: CaCO3 particles, prepared by colloidal crystallization of CaCl2 and Na2CO3 solutions, were used as micro-templates for LbL deposition of CHI and NaALG. Subsequent to the deposition, templates were decomposed to obtain hollow microcapsules. Prepared microcapsules were subjected to physicochemical evaluations, drug release and stability studies.Results and major conclusion: Though CaCO3 particles possessed a rough and irregular surface, prepared hollow microcapsules were spherical in shape, having smooth surface and regular thickness. Following deposition of each layer, alternating values of zeta potential were observed, indicating the formation of multilayered films. Microcapsules with 5 bilayers, i.e. (CHI/NaALG)5 provided 39% entrapment efficiency and exhibited a controlled release behavior, lasting up to 24 hrs. An improvement in drug release rate and stability profile of the formulation was observed by increasing the number of deposition steps and performing the crosslinking of polyelectrolytes. This study showed that the prepared formulation could promisingly be utilized as controlled delivery vehicle for INH.

Background: The emergence of drug-resistant strains of Mycobacterium tuberculosis (MTB) is an increasing problem in developed and developing countries. The aims of the present study were to identify various types of mutations in katG region from 28 MDR strains isolated from sputum of tuberculosis patients.Materials and Methods: Twenty-eight rifampin-resistant strains isolated from sputum of patients with active pulmonary tuberculosis were obtained from various geographic regions of Iran. Drug susceptibility was determined by using the BACTEC system. DNA extraction, standard PCR identification, katG gene amplification, DNA sequencing and analysis were done.Results: There was no mutation in 2 strains. In 20 strains, mutation was shown to be in codon 315. Three types of mutations were detected consisting of AGC®ACC (Ser®Thr) (80%), AGC®AGG (Ser®Arg) (5%) and AGC®AAC (Ser®Asn) (15%). Furthermore, one type of mutation was seen in codons 311, 299, and 323. Twelve strains showed one mutation in codon 315 (46%), 7 strains 2 mutations (27%), 5 isolate 3 mutations (19%) and in 2 strains 4 mutations (8%) were observed in different codons. Nine silent mutations was demonstrated in codon 311 (GAC®TAC).Conclusion: This research demonstrated that mutations were mostly seen in codons 315 and 299 indicating resistance to Isoniazide.

Isoniazid (INH) and rifampicin (RFP) are primary antituberculosisdrugs. Hepatotoxicity is one of the most criticalside effects of these drugs (1). Cessation of INH and RFP, due to hepatotoxicity in patients with tuberculosis, maylead to treatment failure. Therefore, we need novel protectiveagents against the hepatotoxic side effects of INH andRFP.

Background: Recently, advances have emerged in medicine and pharmacotherapeutics, providing novel treatments for tuberculosis (TB). It is noteworthy that long-term drug consumption for TB treatment often leads to hepatotoxicity, which can have serious or even fatal side effects. Thus, many studies have focused on the assessment of the hepatoprotective effects of betaine, a glycine derivative. This study aimed at evaluating the eff, ects of betaine to explore the underlying biochemical mechanisms of hepatotoxicity in rats, using combined Isoniazid (INH) and rifampicin (RMP). Methods: We used an animal model to induce hepatotoxicity with combined INH-RMP and to determine the protective effects of betaine at three doses of 125, 250 and 500 mg/kg. Results: Treatment with INH and RMP led to a significant upregulation of hepatic damage markers, along with marked alteration in the histopathological lesions. The results after the use of betaine were found to be satisfactory at 500 mg/kg comparable to silymarin (200mg/kg). The hepatotoxicity was also found to be associated with generation of reactive oxygen species (ROS) and oxidative stress, indicating the deterioration of the antioxidant defense system in the liver. However, pretreatment with betaine seemed to ameliorate the INH-RMP-induced hepatotoxicity, along with marked down-regulation of oxidative stress and hepatotoxicity markers. Conclusion: The study findings indicated that treatment with betaine may help alleviate the INHRMP-induced liver pathology. This was evident by the reduced inflammation and oxidative stress via mitochondrial GSH regeneration, ROS inhibition, and protection of mitochondria complex II. Further studies are warranted to investigate the validity of these outcomes.