Milton Prabu

Annamalai University, Zoology, Faculty Member

University of Madras chennai, Zoology, Faculty Member

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I am working as an Associate professor in the Department of Zoology, University of Madras. At present, i am involving in the toxicological research about the organ toxic effects of heavy metals and their chelation by phytoconstituents. I have published more than 78 international peer-reviewed papers, with a total impact factor 96. 28 and I have organized two national conferences and workshops in environmental toxicology and running one UGC Major research project in toxicology.
Phone: +919842325222
Address: Assistant Professor,department of zoology Annamalai university,chidambaram,Tamilnadu-28002 India

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Papers by Milton Prabu

Ameliorative effect of curcumin against cadmium induced hepatotoxicity in rats

Abstract Curcumin, a major constituent of turmeric (Curcuma longa) which has been reported to hav... more

Effect of heavy metal mercury on histological changes in the fat body of adult male Laccotrephes ruber (Linn.) (Heteroptera: Nepidae)

Journal of Experimental Zoology, India, 2008

Impact of phytopesticide, nimbecidine on histological changes in the seminal vesicle of adult male Odontopus varicornis (Dist.) (Hemiptera: Pyrrhocoridae)

Asian Journal of Environmental Science, 2008

The male reproductive system of Odontopus vericornis consists of a pair of testis, seminal vesicl... more The male reproductive system of Odontopus vericornis consists of a pair of testis, seminal vesicle, vasadeferentia, a common ejaculatory duct, an erection fluid reservoir (ambulla), a pair of short oval shaped accessory glands opening into the reservoir and an adeagus. The seminal vesicle showed remarkable changes in the insects treated with phytopesticide, nimbecidine (25 ppm median lethal concentration). In treated insects shows a highly disintegrated epithelial cells with weakly stained cytoplasm and nuclei with many cytoplasmic vacuoles.

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Impact of phytopesticide nimbecidine in the MARG's of adult male, Odontopus varicornis (Dist.) (Hemiptera: Pyrrhocoridae) in relation to reproduction

Journal of Experimental Zoology, India, 2007

Protective role of vitamin C (ascorbic acid) and E (α-tocopherol) against cadmium induced hepatotoxicity in rats

Asian Journal of Environmental Science, 2008

This study was carried out to evaluate the effect of dietary vitamins C (ascorbic acid) and E (α-... more

In Vivo and In Vitro Antioxidative Efficacy of Naringenin on Cadmium -Induced Toxicity in Rats

Research & Reviews: A Journal of Toxicology, Sep 1, 2014

The aim of the study was to investigate the in vivo circulating antioxidants level such as vitami... more The aim of the study was to investigate the in vivo circulating antioxidants level such as vitamin C, vitamin E and GSH in Cadmium (Cd) induced toxic rats and the protective efficacy of naringenin via in vitro free radical scavenging assays. In this investigation cadmium chloride (5 mg/kg body weight (b.w) was administered orally (p.o) for 28 days to induce toxicity. Naringenin was pre-administered orally (50 mg/kg body weight) for 28 days with cadmium chloride. The toxic effect of cadmium was indicated by significantly decreased activities of non-enzymatic antioxidants like reduced glutathione, vitamin C and vitamin E. Treatment with naringenin exhibited a significant (P < 0.05) increase in Cd-induced rats. The free radical scavenging properties of naringenin were investigated with different in vitro methods such as 2, 2 ¢ -diphenyl-1-picrylhydrazyl radical (DPPH•), 2,2’-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) radical (ABTS•+), hydroxyl radical, superoxide anion scavenging activity and reducing power. In addition to that ascorbic acid, butylated hydroxyl toluene was used as the reference antioxidant radical scavenger compounds. Among the different concentration, 500 μM of naringenin had significantly effective compared to other concentration in all in vitro assay. Based on these findings naringenin possess potent in vivo and in vitro antioxidant efficacy and also effective free radical scavenger, augmenting its therapeutic value.

Silibinin attenuates arsenic induced alterations in serum and hepatic lipid profiles in rats

To study the protective effect of silibinin against arsenic induced alterations in the serum and ... more To study the protective effect of silibinin against arsenic induced alterations in the serum and hepatic lipid profiles in rats. In this context, the chronic oral exposure of sodium arsenite as the source of arsenic (As) at 5mg/kg/bw with silibinin (SB) 75mg/kg/bw for 28 days. In the present experiment, the elevated levels of serum hepatic markers such as aspartate transaminase (AST), alanine transaminase (ALT),alkaline phosphatise(ALP) and serum cholesterol, triglycerides, low density lipoprotein (LDL), very Low Density Lipoprotein (VLDL), tissue triglycerides and cholesterol with concomitant decrease in serum HDL and tissue phospholipids were observed in As intoxicated rats. Pre-administration of SB with As was found to protect against adverse changes in the serum and hepatic tissue lipid profile in rats. Our results suggest that SB exerts a hypolipidemic effect against arsenic induced toxicity in liver by restoring the altered levels of lipids. The protective effects of SB on serum and liver as evidenced by the clear restoration of lipid profile in rats.

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Epigallocatechin gallate protects fluoride induced neurotoxicity

Fluoride (Fl) exposure engenders neurodegeneration in the brain. The Neuroprotective role of EGCG... more Fluoride (Fl) exposure engenders neurodegeneration in the brain. The Neuroprotective role of EGCG against Fl induced neurotoxicity in rat hippocampus has not yet been explored so far. In this present exploration we focused to witness whether EGCG (40mg/kg) prevents the Fl induced oxidative stress in the brain of rats with special emphasis on hippocampus. Fl (25mg/kg) intoxication for 4 weeks shows decreased neurotransmitters (AChE, NP, DA and 5-HT) in the brain. The oxidative stress markers (ROS, TBARS, NO and PC) were significantly increased with decreased enzymatic (SOD, CAT, GPx, GR, GST, and G6PD) and non-enzymatic antioxidants (GSH, TSH and Vit.C) in Fl intoxicated rat hippocampus. Moreover, Fl intoxicated rats showed an intrinsic and extrinsic pathway mediated apoptosis in the hippocampus of rats. Fl significantly increased the DNA damage as evidenced by increased DNA fragmentation. Furthermore, the toxic impact of Fl on hippocampus was also proved by the immunohistochemical, histological and ultra-structural studies. Pre-administration of EGCG significantly protected the rat brain and hippocampus against Fl ROS by its strong antioxidant and free radical scavenging ability.

Ameliorative effect of selenium on cadmium induced biochemical alterations in Cirrhinus mrigala (Ham.)

Asian Journal of Biological Sciences, 2007

Abstract Heavy metal pollutants are generally discharged in the aquatic environment as a result o... more

Endosulfan-Induced Hepatotoxicity and its Amelioration by Administration of Bamboo (Dendrocalamus Strictus) Seed Extract in Rats

Endosulfan is an important hepatotoxic agent that generates free oxygen radicals in liver and the... more Endosulfan is an important hepatotoxic agent that generates free oxygen radicals in liver and the incidence of toxic injury to the liver tissue in relation to its widespread has been reported. Bamboo is rich in phenolic components which possess various bioactivities and bamboo seed extract was found to have antioxidative properties. Hence, the present study has been designed to assess the protective role of bamboo seed extract against endosulfan induced hepatotoxicity in rat as the endosulfan can persistent to environment where its attributes lead to bioconcentration and biomagnification in certain food chains. For experiments male albino rats weighing 170–190 g were randomly selected and divided into four groups consisting of six rats in each group. The hepatotoxic effects of oral administration of endosulfan (15 mg/kg B.W) and hepato-protective effect of co-administration of bamboo seed extract (90 mg/kg B.W) with endosulfan daily for 10 days, were investigated in rats using serum...

Arsenic-induced biochemical and genotoxic effects and distribution in tissues of Sprague–Dawley rats

Microchemical Journal, 2012

Arsenic (As) is a well documented human carcinogen. However, its mechanisms of toxic action and c... more Arsenic (As) is a well documented human carcinogen. However, its mechanisms of toxic action and carcinogenic potential in animals have not been conclusive. In this research, we investigated the biochemical and genotoxic effects of As and studied its distribution in selected tissues of Sprague-Dawley rats. Four groups of six male rats, each weighing approximately 60 ± 2 g, were injected intraperitoneally, once a day for 5 days with doses of 5, 10, 15, 20 mg/kg bw of arsenic trioxide. A control group was also made of 6 animals injected with distilled water. Following anaesthetization, blood was collected and enzyme analysis was performed by spectrophotometry following standard protocols. At the end of experimentation, the animals were sacrificed, and the lung, liver, brain and kidney were collected 24 h after the fifth day treatment. Chromosome and micronuclei preparation was obtained from bone marrow cells. Arsenic exposure significantly increased (p<0.05) the activities of plasma alanine aminotransferase-glutamate pyruvate transaminase (ALT/GPT), and aspartate aminotransferase-glutamate oxaloacetate transaminase (AST/GOT), as well as the number of structural chromosomal aberrations (SCA) and frequency of micronuclei (MN) in the bone marrow cells. In contrast, the mitotic index in these cells was significantly reduced (p<0.05). These findings indicate that aminotransferases are candidate biomarkers for arsenic-induced hepatotoxicity. Our results also demonstrate that As has a strong genotoxic potential, as measured by the bone marrow SCA and MN tests in Sprague-Dawley rats. Total arsenic concentrations in tissues were measured by inductively coupled plasma mass spectrometry (ICP-MS). A dynamic reaction cell (DRC) with hydrogen gas was used to eliminate the ArCl interference at mass 75, in the measurement of total As. Total As doses in tissues tended to correlate with specific exposure levels.

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Arsenic Induced Oxidative Stress and Its Possible Reversal by Chelation Therapy

ABSTRACT Arsenic (As) is a metalloid listed in group Va of the periodic chart. It exists in natur... more ABSTRACT Arsenic (As) is a metalloid listed in group Va of the periodic chart. It exists in nature in the oxidation states +V (arsenate), +III (arsenite), 0 (arsenic) and −III (arsine). In the aqueous environment inorganic arsenic appears commonly in the oxidation states +V and +III as arsenous acid (As (III)), arsenic acid (As (V)), and their salts. Chronic and acute exposures of arsenic leads to cancer, cardiovascular disease (hypertension and atherosclerosis), neurological disorders, gastrointestinal disturbances, liver disease and renal disease, reproductive health effects, dermal changes and other health disorders and also affects the antioxidant system in the body. Furthermore, reactive oxygen species (ROS)-mediated oxidative damage is a common denominator in arsenic pathogenesis. Formation of free radical such as superoxide radical due to cascade mechanism, combined with glutathione-depleting agents, increases the sensitivity of cells to arsenic toxicity. Formation of ROS/RNS, including peroxyl radicals (ROO•), the superoxide radical, singlet oxygen, hydroxyl radical (OH•) via the Fenton reaction, hydrogen peroxide, the dimethylarsenic radical, the dimethylarsenic peroxyl radical and/or oxidant-induced DNA damage, when both humans and animals are exposed to arsenic. In addition, arsenic induces the formation of oxidized lipids which in turn generate several bioactive molecules (ROS, peroxides and isoprostanes), of which aldehydes [malondialdehyde (MDA) and 4-hydroxy-nonenal (HNE)] are the major end products. Various traditional antidotes are recommended for the present study such as DMSA (meso-2,3-dimercaptosuccinic acid), DMPS(2,3-dimercapto-1-propanesulfonic acid) DMPA (N-(2,3-dimercaptopropyl)-phthalamidic acid) BAL (2,3-dimercapto-1-propanol), Taurine (2-aminoethaesulfonic acid) against arsenic-induced toxicity. Recently, such phyto-antidotes like silibinin, arjunolic acid, vitamin C (ascorbic acid), vitamin E (α-tocopherol) and curcumin have played a major role in arsenic toxicity. Glutathione and antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase showed the protective role against arsenic-induced oxidative stress

Yan Li | Avishay Pelah | ... Epigallocatechin gallate supplementation protects against renal injury induced by fluoride intoxication in rats: Role of Nrf2/HO-1 signaling

Toxicology Reports

Abstract Fluoride intoxication generates free radicals, causing oxidative stress that plays a cri... more Abstract Fluoride intoxication generates free radicals, causing oxidative stress that plays a critical role in the progression of nephropathy. In the present study, we hypothesized that epigallocatechin gallate (EGCG), found in green tea, protects the kidneys of rats treated with fluoride by preventing oxidative stress, inflammation, and apoptosis. Pretreatment of fluoride-treated rats with EGCG resulted in a significant normalization of creatinine clearance and levels of urea, uric acid, and creatinine. Fluoride intoxication significantly increased renal oxidative stress markers and decreased the levels of renal enzymatic and non-enzymatic antioxidants. In addition, renal NO, TNF-α, IL-6 and NF-κB were also increased in the renal tissue of fluoride-treated rats. Further, EGCG pretreatment produced a significant improvement in renal antioxidant status and reduced lipid peroxidation, protein carbonylation and the levels of inflammatory markers in fluoride-treated kidney. Similarly, m...

Diallyl trisulfide ameliorates arsenic induced dyslipidemia in rats

Food Science and Biotechnology, 2015

ABSTRACT Abstract The efficacy of diallyl trisulfide (DATS) against arsenic (As) induced dyslipid... more ABSTRACT Abstract The efficacy of diallyl trisulfide (DATS) against arsenic (As) induced dyslipidemia in the plasma and livers of rats was studied. Oral administration of As [5 mg/kg of body weight (BW)/d] for 4 weeks showed significant (p&lt;0.05) increases in TC, LDL-C, VLDL-C, FFA, PL, and TGs, levels and the activity of HMG-CoA reductase in the plasma and liver with significant (p&lt;0.05) reductions in levels of HDL-C hepatic ubiquinones and activities of LCAT and LPL in the plasma and liver. Oral administration of DATS (80 mg/kg of BW) for 4 weeks in As intoxicated rats significantly (p&lt;0.05) reduced plasma and liver TC, FFA, TGs, VLDL-C, and LDL-C levels, and the activity of HMG-CoA reductase, and significantly (p&lt;0.05) increased the activities of LCAT and LPL and the levels of HDL-C and ubiquinone in the livers of rats. DATS protects against As-induced dyslipidemia in rats.

Molecular Mechanism of Fluoride Induced Oxidative Stress and Its Possible Reversal by Chelation Therapy

Abstract Fluorine (Fl) a member of the halogen family is the most electronegative and reactive of... more Abstract Fluorine (Fl) a member of the halogen family is the most electronegative and reactive of all the elements of Periodic table. Chronic and acute exposures of fluoride leads to cardiovascular disease (hypertension and atherosclerosis), neurological disorders, gastrointestinal disturbances, liver disease, renal disease, reproductive effects, other health disorders and also affects the antioxidant system in the body. Furthermore, reactive oxygen species (ROS)-mediated oxidative damage is a common malady in fluoride pathogenesis. Formation of free radical due to cascade mechanism combined with glutathione-depleting agents increases the oxidation process in the cells and cause damage. Formation of ROS/RNS including peroxyl radicals (ROO•) the superoxide radical, singlet oxygen and hydroxyl radical (OH•) via the Fenton reaction direct DNA damages when both humans and animals are exposed to fluoride. In addition, fluoride induces the formation of oxidized lipids which in turn genera...

Protective role of grape seed proanthocyanidins against cadmium induced hepatic dysfunction in rats

Toxicology Research, 2014

ABSTRACT

Hepatoprotective effect of Andrographis paniculata against cadmium induced toxicity in male wistar rats

Toxicology International, 2008

The present work was carried out to evaluate the hepatoprotective effect of A. paniculata, a popu... more The present work was carried out to evaluate the hepatoprotective effect of A. paniculata, a popular Indian ethnomedicine in the liver of cadmium chloride intoxicated rats. Oral administration of cadmium (5mg/kg body wt.) for 30 days resulted in a significant (p<0.01) elevation of serum aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and bilirubin and the levels of lipid peroxidation marker, malondialdehyde (MDA) in liver. Cadmium also caused a significant reduction in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced the glutathione level in liver. Prior oral administration of A. paniculata extract (100 mg/kg body wt.) with cadmium chloride significantly decreased the serum hepatic marker enzymes viz., AST, ALT, ALP, LDH and the level of bilirubin along with the significant decrease in the levels of lipid peroxidation in the liver. In addition the A.pa...

Ameliorative Potential of Dimethoxy- curcumin: Effect on Lipid Profile and Changes in Tissue Fatty Acid Composi- tion in Arsenic Intoxicated Rats

Arsenic is a well known toxic metalloid which induces a broad spectrum of toxicological effects, ... more Arsenic is a well known toxic metalloid which induces a broad spectrum of toxicological effects, biochemical dysfunctions and dyslipidemia, constituting serious hazard to health. DiMC is sound recognized for its antioxidant, anti-cancer, anti-inflammatory and anti-apoptotic actions. Hence the present study was designed to examine the antihyperlipidemic effect of Dimethoxycurcumin (DiMC) against arsenic induced dyslipidemia in rats. Oral administration of As (5 mg/kg of body weight (BW)/d) for 4 weeks showed significant (p<0.05) elevated levels of TC, LDL-C, VLDL-C, FFA, PL, and TGs, and the activity of HMG-CoA reductase in the plasma and liver with significant (p<0.05) reductions in levels of HDL-C hepatic ubiquinones and activities of LCAT and LPL in the plasma and liver. Pre-administration of DiMC (80 mg/kg of BW) for 4 weeks in As intoxicated rats significantly (p<0.05) reduced plasma and liver TC, FFA, TGs, VLDL-C, and LDL-C levels, and the activity of HMG-CoA reductase...

Melatonin abrogates cadmium induced oxidative stress related neurotoxicity in rats

European review for medical and pharmacological sciences, 2011

BACKGROUND Cadmium is a potent neurotoxic heavy metal, which induces oxidative stress and membran... more BACKGROUND Cadmium is a potent neurotoxic heavy metal, which induces oxidative stress and membrane disturbances in brain. Melatonin is an effective antioxidant and free radical scavenger against oxidative stress. The present study was designed to investigate the neuroprotective efficacy of melatonin in protecting the Cd induced changes in the activity of acetylcholinesterase (AChE), levels of lipid peroxidation, protein carbonyls, non-enzymatic antioxidant, enzymatic antioxidant status, membrane bound ATPases and histopathology in the brain of rats. MATERIALS AND METHODS Twenty four male albino rats were used. Cadmium induced oxidative neurotoxicity was induced by oral administration of Cd for four weeks. Melatonin was pretreated along with Cd for four weeks to assess its neuroprotective activity against Cd intoxication. Rats treated with vehicles alone were used as controls. RESULTS Rats intoxicated with cadmium (5 mg/kg/day) for 4 weeks significantly (p < 0.05) reduced the AChE...

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Iconographies supplémentaires de l'article : Quercetin protects against cadmium-induced biochemical and structural changes in rat liver revealed by FT-IR spectroscopy