Preparation for Human Study of Pesticide Applicators: Sister Chromatid Exchanges and Chromosome Aberrations in Cultured Human Lymphocytes Exposed to Selected Fumigants

Garry, Vincent F.; Nelson, Richard L.; Griffith, Jack; Harkins, Mary E.

doi:10.1002/tcm.1770100104

Cited by 62 publications

(16 citation statements)

References 26 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…But, it was also reported that fumigant applicators were exposed to PH(3) had significantly increased CA and SCE rates in lymphocytes. [22] Our findings also revealed that AIP lead to oxidative damage on cultured human blood cells. In this study, AIP caused increase of TOS level and decrease of TAC level as compared to control group.…”

Section: Discussionsupporting

confidence: 57%

Aluminium phosphide-induced genetic and oxidative damages in vitro: Attenuation by Laurus nobilis L. leaf extract

Türkez

Toğar

2013

Indian J Pharmacol

View full text Add to dashboard Cite

Objective:The present investigation was undertaken to assess the protective effect of Laurus nobilis leaf extract (LNE) against aluminum phosphide (AIP)-induced genotoxic and oxidative damages stress in cultured human blood cells in the presence of a metabolic activator (S9 mix).Materials and Methods:Sister chromatid exchange (SCE) and chromosome aberration (CA) assays were used to assess AlP-induced genotoxicity and to establish the protective effects of LNE. In addition, we determined total antioxidant capacity (TAC) and total oxidative status (TOS) levels in AlP and LNE treated cultures for biomonitoring the oxidative alterations.Results:There was significant increases (P < 0.05) in both SCE and CA frequencies of cultures treated with AlP as compared to controls. Our results also showed that AlP (58 mg/l) caused oxidative stress by altering TAC and TOS levels. However, co-application of LNE (25, 50, 100 and 200 mg/l) and AlP resulted in decreases of SCE, CA rates and TOS level and increases of TAC level as compared to the group treated with AlP alone.Conclusion:The preventive role of LNE in alleviating AlP-induced DNA and oxidative damages was indicated for the first time in the present study.

show abstract

Section: Discussionsupporting

confidence: 57%

Aluminium phosphide-induced genetic and oxidative damages in vitro: Attenuation by Laurus nobilis L. leaf extract

Türkez

Toğar

2013

Indian J Pharmacol

View full text Add to dashboard Cite

show abstract

“…They also considered that the conclusions from these animal experiments could not be extrapolated to human non-conjugators, since these particular individuals are unable to metabolize methyl bromide as quickly as a rodent can [24]. Other studies report pre-carcinogenic sister chromatid exchange and the induction of chromosome aberrations after exposure to methyl bromide [53,54]. …”

Section: Resultsmentioning

confidence: 99%

Prostate cancer and toxicity from critical use exemptions of methyl bromide: Environmental protection helps protect against human health risks

Budnik¹,

Kloth²,

Velasco-Garrido

et al. 2012

Environ Health

View full text Add to dashboard Cite

BackgroundAlthough ozone-depleting methyl bromide was destined for phase-out by 2005, it is still widely applied as a consequence of various critical-use-exemptions and mandatory international regulations aiming to restrict the spread of pests and alien species (e.g. in globalized transport and storage). The withdrawal of methyl bromide because of its environmental risk could fortuitously help in the containment of its human toxicity.MethodsWe performed a systematic review of the literature, including in vitro toxicological and epidemiological studies of occupational and community exposure to the halogenated hydrocarbon pesticide methyl bromide. We focused on toxic (especially chronic) or carcinogenic effects from the use of methyl bromide, on biomonitoring data and reference values. Eligible epidemiological studies were subjected to meta-analysis.ResultsOut of the 542 peer reviewed publications between 1990-2011, we found only 91 referring to toxicity of methyl bromide and 29 using the term "carcinogenic", "neoplastic" or "mutagenic". Several studies provide new additional data pertaining to the mechanistic aspects of methyl bromide toxicity. Few studies have performed a detailed exposure assessment including biomonitoring. Three evaluated epidemiological studies assessed a possible association between cancer and methyl bromide. Overall, exposure to methyl bromide is associated with an increased risk of prostate cancer OR, 1.21; 95% CI (0,98-1.49), P = 0.076. Two epidemiological studies have analyzed environmental, non-occupational exposure to methyl bromide providing evidence for its health risk to the general public. None of the epidemiological studies addressed its use as a fumigant in freight containers, although recent field and case reports do refer to its toxic effects associated with its use in shipping and storage.ConclusionsBoth the epidemiological evidence and toxicological data suggest a possible link between methyl bromide exposure and serious health problems, including prostate cancer risk from occupational and community exposure. The environmental risks of methyl bromide are not in doubt, but also its health risks, especially for genetically predisposed subjects, should not be underestimated.

show abstract

“…It has been reported that malathion induced complex structural chromosomal aberrations in whole human blood cells in the presence of S9 mix [29].…”

Section: Discussionmentioning

confidence: 99%

Impact of isomalathion on malathion cytotoxicity and genotoxicity in human HepaRG cells

Jossé

Sharanek

Savary

2014

Chemico-Biological Interactions

View full text Add to dashboard Cite

Isomalathion is a major impurity of technical grade malathion, one of the most abundantly applied insecticides; however little is known about its hepatotoxicity. In the present study, cytotoxicity and genotoxicity of malathion and isomalathion either individually or in combination, were assessed using the metabolically competent human liver HepaRG cell line. Isomalathion reduced cell viability starting at a 100µM concentration after a 24h exposure. It also significantly induced caspase-3 activity in a dose-dependent manner starting at 5 µM. On the contrary, even at concentrations as high as 500µM malathion affected neither cell viability nor caspase-3 activity.Moreover, co-exposure of both compounds resulted in decreased toxicity of isomalathion. By contrast, malathion and isomalathion either separately or in combination, slightly induced micronuclei formation at low concentrations and had additive genotoxic effects when combined at 25µM. Individually or combined isomalathion directly inhibited activity of carboxyesterases which are involved in detoxication of malathion. In addition, transcripts of CYP2B6 and CYP3A4, two CYPs responsible for malathion phase I metabolism, were strongly induced by the mixture while isomalathion alone only moderately decreased CYP1A2 and increased CYP2B6 transcripts. However, these CYPs were not altered at the protein or activity levels. Taken altogether, our results showed that isomalathion was much more cytotoxic than malathion while both compounds had comparable genotoxic effects in HepaRG hepatocytes at low concentrations and brought further support to the importance of considering impurities and interactions during evaluation of health risks of pesticides.

show abstract

Preparation for Human Study of Pesticide Applicators: Sister Chromatid Exchanges and Chromosome Aberrations in Cultured Human Lymphocytes Exposed to Selected Fumigants

Cited by 62 publications

References 26 publications

Aluminium phosphide-induced genetic and oxidative damages in vitro: Attenuation by Laurus nobilis L. leaf extract

Aluminium phosphide-induced genetic and oxidative damages in vitro: Attenuation by Laurus nobilis L. leaf extract

Prostate cancer and toxicity from critical use exemptions of methyl bromide: Environmental protection helps protect against human health risks

Impact of isomalathion on malathion cytotoxicity and genotoxicity in human HepaRG cells

Contact Info

Product

Resources

About