Amar K. Chandra

Vitamin E-supplementation protect chromium (VI)-induced spermatogenic and steroidogenic disorders in testicular tissues of rats

Excess chromium (Cr) exposure is associated with various pathological conditions including reproductive dysfunction. Generation of oxidative stress is one of the plausible mechanisms behind Cr induced cellular deteriorations. The efficacy of vitamin E to combat Cr induced oxidative damage in adult rat testis has investigated in the current study. Adult male rats exposed to hexavalent Cr (intraperitoneal injection with 0.4 mg K(2)Cr(2)O(7)/ kg bw/day) for 26 days resulted in decreased accessory sex organs weight compared to controls. Development of oxidative stress in testis was evidenced by increased lipid peroxidation along with decreased superoxide dismutase (SOD) and catalase activities than control animals. Marked reduction in the activities of testicular steroidogenic enzymes; Delta(5)3beta-hydroxysteroid dehydrogenase (HSD), 17beta-HSD, serum testosterone and Leutinizing Hormone (LH) levels were observed. However significant increase in serum Follicle Stimulating Hormone (FSH) level was observed with Cr treated group. Histological evaluation of testis revealed degeneration of stage VII spermatogenic cycle along with decrease in epithelial cell height in epididymis and seminiferous tubules; number of different germ cells per seminiferous tubule and seminiferous tubular diameter reduced after Cr exposure. Simultaneous oral supplementation of vitamin E (50mg/kg bw/day) in Cr exposed rats showed less oxidative damage and restored the otherwise altered testicular activities. Epididymal sperm number was also restored in vitamin E-supplemented group than Cr induced rats. This study implicates vitamin E as a possible protective agent against Cr induced spermatogenic and steroidogenic alteration.

Effect of curcumin on chromium-induced oxidative damage in male reproductive system.

Hexavalent chromium, an environmental contaminant, undergoes redox cycling with generation of free radicals inside the biological system. Curcumin, the yellow bioactive component of turmeric has established its antioxidant activities. The present study evaluates possible ameliorating effects of curcumin on potassium dichromate (K(2)Cr(2)O(7)) (hexavalent chromium) induced reproductive toxicity in adult male Sprague-Dawley rats. Three experimental groups, each consisting of eight rats, were treated with 0.4mg K(2)Cr(2)O(7)/kg bw/day, 0.4mg K(2)Cr(2)O(7)/kg bw/day+20mg curcumin/kg bw on every alternate day and 20mg curcumin/kg bw on every alternate day, respectively, for 26 days. Altered testicular histology, reduced sperm count, low testosterone level, decreased accessory sex organs weight, enhanced lipid peroxidation along with reduced SOD and catalase activities were observed following K(2)Cr(2)O(7) exposure while curcumin supplementation along with K(2)Cr(2)O(7) exposure had shown to prevent the altered parameters. The results thus suggest that curcumin may have a protective role against chromium(VI) induced oxidative damage in male reproductive system.

Iodine nutritional status of children in North East India

ObjectiveTo assess the iodine nutritional status of school children in selected areas of Imphal West District of Manipur where endemic goitre and associated iodine deficiency disorders (IDD) are prevalent in the post-salt iodization period.MethodsA total of 961 school children in the age group 6–12 yrs of both sexes were clinically examined for goiter from three study areas-one from rural block and two from urban areas. One hundred twenty urine samples were, analysed for iodine and thiocyanate respectively. One hundred and five edible salt samples were also collected from the households to evaluate the iodine content. Drinking water samples from different sources were collected and iodine level was analysed to study the bioavailability of iodine in the region.ResultsThe total goiter rate was 34.96% (Grade 1–32.15%; Grade 2–2.81%) showing that IDD is a severe public health problem. The median urinary iodine levels in the studied areas were in the ranges from 12.5–17.5 μg/dl indicating no biochemical iodine deficiency in the region. Mean urinary thiocyanate level was 0.839±0.33 mg/dl showing that the people consume sufficient foods containing thiocyanate precursors. About 82% salt samples had iodine level more than 30 ppm and the iodine content in salt samples less than 15 ppm was only about 3% indicating the salt samples at house hold contain adequate iodine.ConclusionIodine content in drinking water samples ranged from 1.8–2.6 μg/l showing that the studied region is environmentally iodine deficient. Inspite of the consumption of adequate iodine, the existing goiter prevalence among school children during post salt iodization phase ensures that environmental factors other than iodine deficiency may have the possible role in the persistence of endemic goiter in the population. The role of thiocyanate in this regard may not be ruled out.

Protection against vanadium-induced testicular toxicity by testosterone propionate in rats

Vanadium is a well recognized industrial hazard known to adversely affect male reproductive functions. The intricate mechanistic aspects of this metal and the role of oxidative stress in the deterioration of testicular functions are investigated in the current study. The experiment also focused on the effects of testosterone propionate in testicular and sperm functions in the rat intoxicated with vanadate. Vanadium exposure resulted in a more prominent spermatogenic arrest and consistently abolished the conversion of round to mature spermatids along with decreased epididymal sperm number and increased percentage of abnormal sperm. This is followed by a precipitous decline in the level of serum testosterone and gonadotropins and consequently the testicular steroidogenic and antioxidant enzymes were inhibited. Vanadium induces degeneration in the genital organs of rats and exhibits high indices of lipid oxidative damage. In response to exogenous testosterone propionate (TP) administration, spermatogonial cell populations remained suppressed, while the spermatogenesis was restored quantitatively. In contrast, the hormone treatment had no effect on the dramatically decreased serum FSH level after vanadate treatment. Moreover, TP could ameliorate the toxicity, as indicated by decreased testicular lipid peroxidation with marginal but significant increase in the activities of all the measured enzymes following vanadate-treatment. Taken together all these studies establish that vanadium is a testicular toxicant that perturbs the male reproductive system adversely. However, hormone replacement therapy by testosterone propionate may provide partial protection. The results suggest the feasibility of using endocrine regimens to impede deleterious effects of vanadium on the male reproductive system.

Amelioration of vanadium-induced testicular toxicity and adrenocortical hyperactivity by vitamin E acetate in rats

Vanadium toxicity is a challenging problem to the health professionals and a cutting-edge medical problem. Vanadium has been recognized as industrial hazards that adversely affect human and animal reproductive health. Since testicular function is exquisitely susceptible to reactive-oxygen species, the present study elucidates the possible involvement of oxidative stress in vanadium-induced testicular toxicity and the prophylactic effects of vitamin E acetate against such adverse effects of vanadium. The study also characterizes the effects of vanadium on rat adrenal steroidogenesis and determines the underlying mechanisms of testicular and adrenal interactions in response to vanadium exposure. Significantly reduced sperm count associated with decreased serum testosterone and gonadotropins level in the vanadium-injected group of rats compared to control substantially proves the ongoing damaging effects of vanadium-induced ROS on developing germ cells. This is in turn reflected in the appreciable increase in testicular lipid peroxidation level and decline in the activities of steroidogenic and antioxidant enzymes. However, oral administration of vitamin E acetate could protect testes from the toxic effects of vanadium. Vanadium also results in adrenocortical hyperactivity, as evidenced by the elevated secretion of glucocorticoids, adrenal gland hypertrophy and increased activity of adrenal Δ53β-HSD. However, reversibility of these alterations in adrenocortical activities was vividly reflected after vitamin E acetate supplementation. All these studies reveal that oxidative stress is the major mechanism of health deterioration and that vanadium can act as a stressor metal causing chronic stress effects through excitation of hypothalamo-pituitary-adrenal axis. However antioxidant support by vitamin E acetate may provide significant protection.

Effect of different doses of un-fractionated green and black tea extracts on thyroid physiology

Tea is a rich source of polyphenolic flavonoids including catechins, which are thought to contribute to the health benefits of it. Flavonoids have been reported to have antithyroid and goitrogenic effect. The purpose of this study was to evaluate whether high doses of green and black tea have a harmful effect on thyroid physiology. Un-fractionated green and black tea extracts were administered orally to male rats for 30 days at doses of 1.25 g%, 2.5 g% and 5.0 g%. The results showed that green tea extract at 2.5 g% and 5.0 g% doses and black tea extract only at 5.0 g% dose have the potential to alter the thyroid gland physiology and architecture, that is, enlargement of thyroid gland as well as hypertrophy and/or hyperplasia of the thyroid follicles and inhibition of the activity of thyroid peroxidase and 5′-deiodinase I with elevated thyroidal Na+, K+-ATPase activity along with significant decrease in serum T3 and T4, and a parallel increase in serum thyroid stimulating hormone (TSH). This study concludes that goitrogenic/antithyroidal potential of un-fractionated green tea extract is much more than black tea extract because of the differences in catechin contents in the tea extracts.

Dietary supplies of iodine and thiocyanate in the etiology of endemic goiter in Tripura.

In the post-salt iodization phase, a study on iodine nutriture status was conducted in Tripura of North East India. The clinical variable of the study was goiter and the biochemical variables were urinary iodine and thiocyanate. Random sampling methodology was followed for selecting the study areas in the State. In each study area, the studied population consisted of school children of both sexes in the age group 6–15 years. The total study areas were 22 and the total number of the population was 10,801. The total number of urine samples were analysed for iodine and thiocyanate were 1,032 (about 10%). The total goiter rate was 21.63%. Population of most of the studied areas had no biochemical iodine deficiency as evidenced by median urinary iodine excretion levels. However, the per capita consumption of iodine of about 40% population was inadequate. A large number of cyanogenic plants (SCN precursors) are used as common vegetables. This study ensures that the existing goiter prevalence in the region could possibly due to non-uniform adequate iodine supply along with the thiocyanate load.

Vanadium-Induced Testicular Toxicity and Its Prevention by Oral Supplementation of Zinc Sulphate

ABSTRACT Transition metal vanadium has been shown to modulate the cellular redox potential and catalyze the generation of reactive oxygen intermediates. Since free radical production and lipid peroxidation are potentially important mediators in testicular physiology and pathophysiology, the present study was conducted to elucidate the vanadium-induced oxidative damages in rat testis and the ameliorative role of zinc sulphate against such adverse effects of vanadium. Adult male rats were dosed for 26 days with daily intraperitoneal injection of 0.4 mg V/kg body weight as sodium metavanadate. One group of rats was treated with zinc sulphate orally simultaneously with vanadium for 26 days, while the other group was treated with zinc sulphate alone. Changes in testicular and accessory sex organ weight, different varieties of germ cells at stage VII of spermatogenic cycle, epididymal sperm count, and enzymatic (Δ53β- HSD, 17β- HSD, SOD, catalase), lipid peroxidation, and hormonal milieu were monitored. Vanadium treatment resulted in a significant increase in the testicular lipid peroxidation and caused a marked inhibition in the activities of antioxidant and steroidogenic enzymes. Histopathological examination revealed inhibition of spermatogenesis and the preferential loss of maturing and elongated spermatids. However, coadministration of zinc sulphate to vanadium-treated animals resulted in normalizing these parameters appreciably, emphasizing the therapeutic potentials of zinc. Taken together, the results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during vanadium exposure may render testis more susceptible to oxidative damage, leading to their functional inactivation. However, zinc sulphate supplementation can be an effective antidote in the treatment of vanadium poisoning.

Influences of Age, Sex and Caste on Goiter Prevalence of the People in Tripura, North East India

Abstract Goiter prevalence of selected population in respect of age, sex and caste was evaluated in the conventional iodine deficient Tripura of north east India during post-salt iodization phase. The study was earned out on 10,801 school-children in the age group 6-15 years of both sexes from randomly selected 22 representative localities. In selected localities, children were clinically examined for goiter categorising them in respect of ages, sexes and castes. Obtained results showed goiter was prevalent at endemic level (more than 5%) in all study localities. With advancement age the rate was found to increase up to the age of JI years in both sexes. However in boys a gradual decline in goiter rate was found and returned to basal level by 15 years while in girls the rate of increase remained steady up to 15 years. Female population was affected more than the male in prevalence and severity. They were exposed under uniform system of iodine supply and dietary goitrogens. however endemic goiter was mostly prevalent in general castes, moderately among scheduled castes and minimum among scheduled tribes These variations might be due to non-uniform environmental adaptability associated with different dietary practices.

Biphasic action of iodine in excess at different doses on ovary in adult rats

Iodine consumption in excess of its recommended levels over a prolonged period of time is well known to cause thyroid disorders. The thyroid hormones on the other hand are responsible in maintenance of the physiology of the reproductive system. Excess iodine intake affects male reproductive physiology. However, the effects of excess iodine on the ovarian structure and function is yet to be established. The present study has thus been undertaken to investigate the effect of excess iodine on the ovarian physiology. Excess iodine was administered through oral gavage in the form of potassium iodide (KI) for duration of 60days, at two different doses. The doses used were 100 EI, i.e., 100 times more than the recommended level but tolerable to the thyroid gland and 500 EI, i.e., 500 times more than the recommended level that altered thyroid physiology. The animals were divided into three groups, one control group, and the other two receiving two separate doses (100 EI and 500 EI) of excess KI. Estrous cyclical changes, ovarian morphological changes, ovarian iodine accumulation and ovarian steroidogenic enzyme activities were analysed. The thyroid functional status was studied from the serum thyroid hormones levels. The overall results revealed a biphasic action of excess iodine that depends on its dose. At 100 EI, excess iodine did not alter thyroid physiology but lead to the development of a hypoestrogenic state. There was an increased accumulation of iodine in the ovary with decreased activity of ovarian steroidogenic enzymes and lowered serum estradiol levels. However, at 500 EI, excess iodine developed a hyperthyroid condition, which further leads to a hyperestrogenic state. There was an increased activity of serum steroidogenic enzymes as well as elevated serum estradiol levels. Fertility index was zero in both the 100 EI and 500 EI treated groups of experimental animals. Thus excess iodine (100 EI) ingestion within tolerable range though maintained a euthyroid condition yet developed a state of hypofunctioning ovary. Conversely, excessive iodine (500 EI) is intolerable to thyroid, develops a hyperthyroid condition that leads to a hyperfunctioning ovary. Therefore prolonged exposure of iodine in excess exerts biphasic mode of action depending on the dose in female reproductive physiology and both the doses used in this study affected fertility equally.