Experimental Selenium Toxicity in Guinea Pigs: Biochemical Studies

Das, P. M.; Sadana, J. R.; Gupta, Rashmi; Kumar, K. E.

doi:10.1159/000177521

Cited by 7 publications

(2 citation statements)

References 16 publications

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“…The resultant hypoproteinaemia in the selenium treated birds was possibly because of its decreased synthesis by the degenerated and / or necrotic liver which was evident in necropsy finding. Similar finding were also reported by Das et al (1989b) in the selenium treated birds. It was found that considerable elevation in the values of BUN in the birds of group A as compared to group B and C birds, but the difference were not significant.…”

Section: Lungssupporting

confidence: 91%

Histopathological alterations of selenium toxicity induced in broiler (Birds)

Gautam

Kumar

Sinha

2017

IJAR

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A study was conducted to determine the pathological toxic effect of selenium (Sodium selenite). A total number 120 one day old White Leghorn (WLH) healthy broiler birds were randomly divided into A, B and C groups. Each group contain 40 birds daily administration of sodium selenite @ 30ppm and @ 15 ppm in group A and B, respectively and group C was given plain drinking water daily for 42 days and kept as control. Macroscopically and microscopically revealed varying degrees of congestion and haemorrhages in lungs, liver, kidneys, heart and intestine in selenium treated birds. The bursa of Fabricius showed depletion of lymphoid cells between the interfollicular spaces. A significant (P less than 0.05) decrease in the haemoglobin and packed cell volume was noticed in both the selenium fed groups but the total erythrocyte count remain unchanged. Biochemical parameter revealed slight decline in their activity of serum ALT and AST and increased level of BUN and creatinine in group A and B as compared to group C, suggesting some degree of renal dysfunctioning.

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Section: Lungssupporting

confidence: 91%

Histopathological alterations of selenium toxicity induced in broiler (Birds)

Gautam

Kumar

Sinha

2017

IJAR

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“…For example, selenium and zinc levels in Taiwan and Bangladesh are among the lowest worldwide ( Lin and Yang 1988 ), and poor dietary selenium has been suggested as an underlying factor for arsenic and cancer in Bangladesh and West Bengal in India ( Spallholz et al 2004 ). In guinea pigs, selenium and arsenic counteract each other in glucose metabolism ( Das et al 1989 ), and the joint effect of high arsenic and low selenium could play a role in diabetes development. Exposure to arsenic, selenium, other nutrients, and other diabetes risk factors were not measured in epidemiologic studies.…”

Section: Discussionmentioning

confidence: 99%

Arsenic Exposure and Type 2 Diabetes: A Systematic Review of the Experimental and Epidemiologic Evidence

Navas‐Acien

Silbergeld

Streeter

et al. 2006

Environ Health Perspect

303

193

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Chronic arsenic exposure has been suggested to contribute to diabetes development. We performed a systematic review of the experimental and epidemiologic evidence on the association of arsenic and type 2 diabetes. We identified 19 in vitro studies of arsenic and glucose metabolism. Five studies reported that arsenic interfered with transcription factors involved in insulin-related gene expression: upstream factor 1 in pancreatic β-cells and peroxisome proliferative-activated receptor γ in preadipocytes. Other in vitro studies assessed the effect of arsenic on glucose uptake, typically using very high concentrations of arsenite or arsenate. These studies provide limited insight on potential mechanisms. We identified 10 in vivo studies in animals. These studies showed inconsistent effects of arsenic on glucose metabolism. Finally, we identified 19 epidemiologic studies (6 in high-arsenic areas in Taiwan and Bangladesh, 9 in occupational populations, and 4 in other populations). In studies from Taiwan and Bangladesh, the pooled relative risk estimate for diabetes comparing extreme arsenic exposure categories was 2.52 (95% confidence interval, 1.69–3.75), although methodologic problems limit the interpretation of the association. The evidence from occupational studies and from general populations other than Taiwan or Bangladesh was inconsistent. In summary, the current available evidence is inadequate to establish a causal role of arsenic in diabetes. Because arsenic exposure is widespread and diabetes prevalence is reaching epidemic proportions, experimental studies using arsenic concentrations relevant to human exposure and prospective epidemiologic studies measuring arsenic biomarkers and appropriately assessing diabetes should be a research priority.

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