Constitutional, organopathic and combined homeopathic treatment of benign prostatic hypertrophy: a clinical trial.

BACKGROUND: Benign Prostatic Hypertrophy (BPH) is common in older men. This study compared homeopathic treatment strategies using constitutional medicines (CM) or organopathic medicines (OM) alone or in combination (BCOM) in patients suffering from BPH. METHODS: 220 men aged 30-90 years were recruited in Odisha, India. Patients presenting symptoms of prostatism, with or without evidence of bladder outflow obstruction were included in the study. Patients with serum prostate specific antigen (PSA)> 4 nmol/mL, malignancy, complete urine retention, stone formation and gross bilateral hydronephrosis were excluded. Patients were sequentially allocated to OM, CM or BCOM. The main outcome measure was the International Prostate Symptom Score (IPSS). RESULTS: 73, 70 and 77 patients respectively were sequentially allocated to OM, CM or BCOM. 180 patients (60 per group) completed treatment and were included in the final analysis. Overall 85% of patients showed improvement of subjective symptoms such as frequency, urgency, hesitancy, intermittent flow, unsatisfactory urination, feeble stream, diminution of residual urine volume but there was no reduction in prostate size. Treatment response was highest with BCOM (38.24%) compared to OM (31.62%) and CM (30.15%). Effect sizes were highest for the decrease in IPSS, residual urine volume and urinary flow rate.

Curcumin and vitamin E modulate hepatic antioxidant gene expression in PTU-induced hypothyroid rats.

In the present study, regulatory role of vitamin E and curcumin on antioxidant gene (AOG) expression in hypothyroid rat liver is reported. Adult male rats were rendered hypothyroid by administration of 0.05 % 6-propyl-thiouracil in their drinking water, while vitamin E (200 mg/kg body weight) and curcumin (30 mg/kg body weight) were supplemented orally for 30 days. Expression of antioxidant genes (Cu/Zn-superoxide dismutase; SOD1, Mn superoxide dismutase; SOD2, catalase; CAT, glutathione peroxidase; GPx1 and glutathione reductase; GR) was evaluated using RT-PCR and Western blot analyses. The activities of antioxidant enzymes were measured in mitochondrial fraction (MF) and post-mitochondrial fraction (PMF) of rat liver. In addition measurement of glutathione redox status was also carried out in both the fractions. The enhanced transcripts of CAT, GPx1 and GR in hypothyroid rat liver were alleviated by administration of vitamin E and curcumin. Elevated levels of translated product of all AOGs in hypothyroid group were remained unchanged after antioxidant administration. However, enhanced SOD1, GPx1 and decreased GR activities in PMF were normalized by vitamin E and curcumin. Similarly the increased SOD2, GPx1 and decreased CAT activities in MF were also normalized by vitamin E and curcumin supplementation. Administration of vitamin E and curcumin enhanced mitochondrial GSH level; whereas the enhanced GSH level in PMF of hypothyroid rats was alleviated by vitamin E. Thus it can be concluded that besides the antioxidant role of vitamin E and curcumin, they also regulate hepatic antioxidant gene expression in hypothyroid rats.

Alleviation of enhanced oxidative stress and oxygen consumption of L-thyroxine induced hyperthyroid rat liver mitochondria by vitamin E and curcumin.

In the present study, the role of vitamin E and curcumin on hyperthyroidism induced mitochondrial oxygen consumption and oxidative damage to lipids and proteins of rat liver are reported. Adult male rats were rendered hyperthyroid by administration of 0.0012% l-thyroxine in their drinking water, while vitamin E (200 mg/kg body weight) and curcumin (30 mg/kg body weight) were supplemented orally for 30 days. Hyperthyroidism induced elevation in serum aspartate aminotransferase and alanine aminotransferase activities were reduced significantly in response to vitamin E and curcumin treatment. On the other hand, effects of vitamin E and curcumin on hyperthyroidism induced hepatic complexes I and II mediated respiration were found to be different. While curcumin administration ameliorates hyperthyroidism induced state 3 and state 4 respiration in complex I, vitamin E treatment was effective only in reducing state 4 respiration of complex I. On the contrary, curcumin administration was ineffective in modulating hyperthyroidism induced complex II respiration, but vitamin E treatment to hyperthyroid rats resulted in augmentation of complex II respiration both at state 3 and state 4 level. Moreover, vitamin E and curcumin treatment resulted in alleviation of hyperthyroidism induced lipid peroxidation. Enhanced protein carbonylation in hyperthyroid rats is decreased only in response to simultaneous supplementation of vitamin E and curcumin. Above findings suggest that both vitamin E and curcumin have differential regulation on complexes I and II mediated mitochondrial respiration and have a protective role against L-thyroxine induced hepatic dysfunction and oxidative stress.

Modulation of antioxidant defences in digestive gland of Perna viridis (L.), on mercury exposures.

Sub-lethal effects of mercury exposure (110th of LC(50), i.e. 0.045 mg l(-1)) for 5, 10 and 15 d was investigated on oxidative stress parameters and antioxidant defences in digestive gland of Perna viridis. In addition to this an in vitro effect of mercury single and supplemented with reduced glutathione on lipid peroxidation was studied. Increased lipid peroxidation (during first 10 days and also during in vitro exposures), protein carbonyl and hydrogen peroxides (from 5th till last day of exposure) indicate the resultant oxidative stress in the mercury exposed specimen. DNA damage (F-value) response although less distinct on 5th and 15th d, its low values on 10th d and significant correlation with hydrogen peroxide suggests the toxic role of free radicals towards DNA integrity. Superoxide dismutase, which remains low initially (5th d) and increases later suggests its immediate response against superoxide radical. Higher activities of catalase, glutathione peroxidase and glutathione reductase on 15th d and glutathione-S-tranferase from 10th d onwards suggests the adaptive behaviour of the tissue against oxyradicals. Increasing levels of non-enzymatic antioxidant molecules, such as reduced glutathione and ascorbic acid indicated its involvement in counteracting oxidative damage. Further role of reduced glutathione in reducing Hg toxicity is evident in in vitro experiments where lipid peroxidation remains low in mercury concentrations supplemented with reduced glutathione. The elevated levels of metallothionein from 5th to 10th d suggest involvement of this protein in detoxification of reactive oxygen species and toxic metal. The above results suggest that both enzymatic and non-enzymatic antioxidants play an important role in protecting cell against Hg toxicity, which can be used as a biomarker of metal contamination in aquatic environment.

Effects of hypothyroidism induced by 6-n-propylthiouracil and its reversal by T3 on rat heart superoxide dismutase, catalase and lipid peroxidation.

The present study critically evaluates the effects of hypothyroid and hyperthyroid states on lipid peroxidation and two enzymes of active oxygen metabolism, namely superoxide dismutase (SOD) and catalase (CAT) in the rat heart mitochondrial and post-mitochondrial fractions. Lipid peroxidation, an index of oxidative stress, was elevated in the heart tissue in hypothyroid state but reduced upon T3 supplementation. Hyperthyroidism registered increased SOD activity in post-mitochondrial fraction. Mitochondrial SOD activity was reduced in hypothyroid state, which was further reduced by T3 administration. In contrast, different thyroid states had no effect on catalase activity in the mitochondrial fraction. The hypothyroid state however, significantly augmented catalase activity in post-mitochondrial fraction. The results suggest that the antioxidant defence status of cardiac tissue is well modulated by thyroid hormone.