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

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Abstract

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.

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Abbreviations

ROS:

Reactive oxygen species

V:

Vanadium

i.p.:

Intraperitoneal

VEA:

Vitamin E acetate

ASg:

Type A spermatogonia

pLSc:

Preleptotene spermatocytes

mPSc:

Mid pachytene spermatocytes

7Sd:

Step 7 spermatids

LH:

Luteinizing hormone

FSH:

Follicle stimulating hormone

HSD:

Hydroxysteroid dehydrogenase

NAD:

Nicotinamide adenine dinucleotide phosphate

LPO:

Lipid peroxidation

TBARS:

Thiobarbituric acid reactive substances

MDA:

Malondialdehyde

SOD:

Superoxide dismutase

CAT:

Catalase

EDTA:

Ethylenediamine tetraacetic acid

BSA:

Bovine serum albumin

HPA:

Hypothalamo-pituitary-adrenal

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Acknowledgment

The authors thank Dr. Syed N. Kabir, Scientist, Cell Biology & Physiology Division, Indian Institute of Chemical Biology (IICB), Kolkata, India for his help in conducting RIA of FSH and LH.

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Authors and Affiliations

  1. Endocrinology and Reproductive Physiology Laboratory, Department of Physiology, University College of Science & Technology, University of Calcutta, 92, Acharya Prafulla Chandra Road, Kolkata, 700 009, West Bengal, India

    Amar K. Chandra, Rituparna Ghosh & Aparajita Chatterjee

  2. Department of Physiology, Gurunanak Institute of Dental Science & Research, Kolkata, India

    Mahitosh Sarkar

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  1. Amar K. Chandra
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  2. Rituparna Ghosh
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  3. Aparajita Chatterjee
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Correspondence to Amar K. Chandra.

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Chandra, A.K., Ghosh, R., Chatterjee, A. et al. Amelioration of vanadium-induced testicular toxicity and adrenocortical hyperactivity by vitamin E acetate in rats. Mol Cell Biochem 306, 189–200 (2007). https://doi.org/10.1007/s11010-007-9569-4

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