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Aluminum phosphide (AlP) is a cheap, effective and commonly used pesticide. However, unfortunately, it is now one of the most common causes of poisoning among agricultural pesticides. It liberates lethal phosphine gas when it comes in contact either with atmospheric moisture or with hydrochloric acid in the stomach. The mechanism of toxicity includes cellular hypoxia due to the effect on mitochondria, inhibition of cytochrome C oxidase and formation of highly reactive hydroxyl radicals. The signs and symptoms are nonspecific and instantaneous. The toxicity of AlP particularly affects the cardiac and vascular tissues, which manifest as profound and refractory hypotension, congestive heart failure and electrocardiographic abnormalities. The diagnosis of AlP usually depends on clinical suspicion or history, but can be made easily by the simple silver nitrate test on gastric content or on breath. Due to no known specific antidote, management remains primarily supportive care. Early arrival, resuscitation, diagnosis, decrease the exposure of poison (by gastric lavage with KMnO4, coconut oil), intensive monitoring and supportive therapy may result in good outcome. Prompt and adequate cardiovascular support is important and core in the management to attain adequate tissue perfusion, oxygenation and physiologic metabolic milieu compatible with life until the tissue poison levels are reduced and spontaneous circulation is restored. In most of the studies, poor prognostic factors were presence of acidosis and shock. The overall outcome improved in the last decade due to better and advanced intensive care management. [ABSTRACT FROM AUTHOR]

Background: Evidence suggests that mitochondrial dysfunction stimulates the production of reactive oxygen species (ROS) that promote neural cell death in stroke and in Parkinson's disease. The sites of mitochondrial ROS production are not established but are generally believed to be located within the electron transport chain.Aims: We studied the mitochondrial respiratory chain enzymes function from human circulating lymphocytes.Setting and Design: Open study.Materials and Methods: Forty patients with Parkinson's disease (PD) with 30 age-matched control subjects were selected in this study. The patients had received no treatment before the study was conducted.Statistical Analysis: The data from patients and controls were compared using two-tailed student's t-test and values were expressed as means +/- standard deviation (SD).Results: Respiratory complex I + III and IV activities were significantly lower (P < 0.001) in patients than in control subjects.Conclusions: The use of lymphocytes for investigating the respiratory chain enzymes provides an easy, noninvasive method to assess mitochondrial function in patients with PD. Furthermore, our study supports the hypothesis that a biochemical defect in the respiratory chain may be involved in the pathogenesis of PD. [ABSTRACT FROM AUTHOR]

Objective: Present study was carried out to evaluate effect of esomeprazole on the pharmacokinetics of carbamazepine in rabbits. Materials and Methods: Study was conducted at Department of Pharmacology, Postgraduate Institute of Medical Education and Research from March to October 2007. In a parallel design study, carbamazepine 40 mg/kg/day was given orally for 14 days. On day 15, blood samples were taken at various time intervals between 0 and 24 hours. In esomeprazole group, carbamazepine was administered for 14 days as above. On day 8, esomeprazole2.8 mg/kg/day along with carbamazepine 40 mg/kg/day was administered till 14 days and blood samples were drawn on 15th day. Plasma levels of carbamazepine were assayed by high-performance liquid chromatography and pharmacokinetic parameters were calculated. Results: In all groups there was a decrease in the AUC0-24 when carbamazepine was coadministered with esomeprazole. The decrease in AUC0-24 (22.78 ± 4.71 to 10.46 ± 2.29), Cmax (2.76 ± 0.77 to 1.412±1.08), Tmax (2.83 ± 0.17 to 3 ± 0.40) was statistically significant (P < 0.05) when esomeprazole was given along with carbamazepine. Additionally, absorption and elimination constant were also altered significantly. Conclusions: These results suggest that concomitant use of esomeprazole alters the pharmacokinetics of carbamazepine. Confirmation of these results in human studies will warrant changes in carbamazepine dose or frequency when esomeprazole is coadministered. [ABSTRACT FROM AUTHOR]

Aim: The present study was designed to study the effect of cytochrome P450 (CYP) modulators on the occurrence of cataract using male Sprague-Dawley rats weighing 40:50 gm. Materials and Methods: Macroscopical examination of the lens isolated from rats pretreated with diltiazem (30 mg/kg; once daily; PO) showed delayed occurrence of cataract while pioglitazone (3.8 mg/kg; once daily; PO) pretreatment demonstrated an early cataract. Results and Conclusion: A delayed occurrence of cataract with diltiazem (CYP inhibitor) and an early onset of cataract with pioglitazone (CYP inducer) indicate that a cytochrome P450 mediated pathway may affect the initiation of cataract but not the maturation pattern. [ABSTRACT FROM AUTHOR]

A response by Kavitha S. Nair, Kirti V. Patel, Tejal R. Gandhi to a letter to the editor about their article "Is cytochrome modulation the new frontier for decreasing the risk of cataract?" in the 2009 issue is presented.

A letter to the editor is presented in response to the article "Is cytochrome modulation the new frontier for decreasing the risk of cataract?" by KS Nair, KV Patel and TR Gandhi in the 2009 issue.

A letter to the editor is presented in response to the article "Is cytochrome modulation the new frontier for decreasing the risk of cataract?," by Kavitha S. Nair and colleagues in the April 2009 issue.

Genotypes of the drug-metabolizing enzyme CYP2D6 influence plasma levels of 25% of commonly prescribed drugs. This is the first study in India to investigate the genotype-phenotype relationship of CYP2D6.~Background~Background~To study the influence of some CYP2D6 genotypes on the metabolism of its substrate dextromethorphan in healthy South Indian volunteers and to assess the contribution of the CYP2D6*10 and CYP2D6*4 alleles.~Aim~Objective~Twenty-six subjects from a previous CYP2D6 genotyping study of healthy volunteers were included for phenotyping in this study. Selected volunteers belonged to any one of three genotype groups:Group I - two normal activity alleles, Group II - one reduced activity allele and one normal activity allele and Group III - one loss of function allele along with either a wild type or reduced activity allele. Volunteers were phenotyped for the CYP2D6 enzyme using dextromethorphan as probe drug. Concentrations of the parent drug and metabolite dextrorphan were estimated using high performance liquid chromatography. Metabolic ratios were calculated as the ratio of parent drug to metabolite in 0-8h urine samples.~Materials and Methods~Methods~Metabolic ratios from each genotype group were compared using the Mann-Whitney test at 5% significance, to observe their difference between genotype groups.~Statistical Analysis~Methods~The mean metabolic ratios+/-SD in Groups I, II and III were 0.0039+/-0.0031, 0.0032+/-0.0017 and 0.0391+/-0.0331 respectively. The mean metabolic ratio of Group III was significantly higher when compared with Groups I or II. In heterozygous individuals, the *1 or *2 alleles compensated for the reduced enzyme activity due to the *10 allele. However, if a heterozygous individual had a *4 allele, the reduced enzyme activity could not be compensated by the *1 or *2 alleles.~Results~Results~The CYP2D6 enzyme activity was found to be decreased in individuals carrying *4 or *5 alleles. The *1 or *2 allele could compensate for the reduced function due to *10 allele, but not for the loss of function due to *4 allele.~Conclusions~Conclusions [ABSTRACT FROM AUTHOR]